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Just the flakes: The relation between dandruff and eczema

October is national eczema awareness month, so why are we bringing up dandruff? Well, that’s because dandruff is the result of scalp eczema, also known as seborrheic dermatitis. It may also appear on the scalp as scaly, dry reddish patches that may even turn to scabs.

Busy executive, Eric, who travels extensively, noticed dry flakes on his dark clothing, but had no time to see a dermatologist. He starting using an over-the-counter dandruff shampoo, which helped a bit at first but didn’t altogether clear things up – and then he noticed flaking skin near his nose too.

Seborrheic dermatitis is a chronic form of eczema that can go through remissions and flares. It affects areas of the body where there are oil-producing glands. In addition to the scalp, those oily areas include the face (particularly around the nose), upper back, and upper chest. With this form of eczema, there is an overgrowth of yeast fungi that causes inflammation on the skin. It is not contagious but can affect persons of any age. In infants whose scalps are affected, it is referred to as “cradle cap.”

Triggers can include:

  • Stress
  • Cold, dry weather
  • Hormonal changes
  • Harsh detergents, soaps, and cosmetic products

For Eric, his triggers were definitely a stressful, busy work and travel schedule combined with spending extended time on airplanes, in airports, and inside air-conditioned office buildings.

Treating Scalp Eczema and Dandruff

Getting a diagnosis from a trained dermatologist is ideal, since the condition can be confused with others such as psoriasis or atopic dermatitis. Treatments will vary based on the severity of the condition and are best prescribed by a dermatologist, but most cases will show clear up in a few weeks after starting treatment.

Eric ultimately tried an online visit with a dermatologist on DermatologistOnCall. He was surprised to learn his diagnosis was actually a chronic form of eczema, and he received a treatment plan for both short-term resolution and directions on how to manage the condition over the long term.

Watch Eric tell his story – and you can have an online dermatology visit any time:

What’s the connection between dandruff and eczema?


Are dandruff and eczema the same or different? Let’s find out if these two conditions are connected.

1. What is dandruff?
2. What is eczema?
3. Dandruff vs. eczema
4. How to treat dandruff and scalp eczema?

When you scratch your scalp and notice flakes, “dandruff” is the first thing that comes to your mind. However, an irritated scalp does not necessarily mean dandruff, it can be a sign of scalp eczema as well. Figuring out what’s causing these flakes plays a vital role in helping you seek the right treatment. Considering they share similar symptoms, you may be wondering – are dandruff and eczema related?

Let’s find out.

What is dandruff?

Contrary to popular belief, dandruff does not occur due to dryness (dry scalp is a different condition altogether). Instead, you have to deal with yellowish-white, oily flakes because your scalp is producing too much sebum. Malassezia globosa, the microbe present on everyone’s scalp, feeds on the sebum and produces a by-product called oleic acid. Though oleic acid is harmless, some people are allergic to this by-product, making their bodies react to this irritant in the form of dandruff. Severe dandruff, also known as Seborrhoeic Dermatitis, is often triggered by stress, cold and dry weather, and hormonal changes.

What is eczema?

When the eczema affects the scalp, it causes patches of skin on the scalp to become red, flaky, and itchy. It can also affect other parts of the body, such as the nose, face, eyebrows, and eyelids, and make the skin greasy, waxy, or blistered. Atopic Dermatitis and Contact Dermatitis are some of the most common types of eczema.

There aren’t any exact causes of eczema but genes, hormones, stress, and illnesses are known to trigger scalp eczema. The symptoms of eczema include:

• Flaking skin
• Swelling
• Itchiness
• Burning
• Redness
• Scaly patches

Dandruff vs.

eczema

Seborrhoeic dermatitis is a chronic form of eczema, that goes through remissions and flare-ups. When eczema is triggered, it can get worsened by a combination of otherwise normal skin properties. When your scalp produces more sebum, it causes an overgrowth of the skin fungus called Malassezia globosa that feeds on sebum. It irritates the sebaceous glands of the scalp and triggers an immune response that causes scaly rashes on the scalp. So, to sum it up, dandruff is a symptom of scalp eczema.

How to treat dandruff and scalp eczema?

The treatment for dandruff and eczema depends on how severe the conditions are. It includes using the right hair products and making essential lifestyle changes that can actively keep the triggers at bay. Here’s what you should do:

  • Choose the right hair products

    To prevent dandruff and keep eczema flare-ups at bay, you need shampoos that contain anti-dandruff active or selenium sulphide. Try Head & Shoulders Clean & Balanced Shampoo that gives you seven major benefits: fights dry scalp, relieves irritation, calms itchy scalp, reduces redness (associated with dandruff), great scent, controls flaky scalp, and leaves hair feeling great. Formulated using HydraZinc, this anti-dandruff shampoo cares for your scalp and leaves your hair feeling soft and manageable. Pair this shampoo with Head & Shoulders Clean & Balanced Conditioner to lock in the immense dandruff-fighting power and keep your hair clean and healthy.
    For severe dandruff that’s caused by eczema, you can try Head & Shoulders Clinically Proven Solutions Scalp Relief Shampoo that’s formulated with selenium sulphide to target severe, stubborn dandruff. Clinically proven to control itching, flaking and soothe an irritated scalp, this gentle formula shampoo is ideal for daily use.

  • Lifestyle changes

    There’s no permanent cure for scalp eczema but following certain lifestyle changes can help keep the flare-ups away. You need to identify the triggers that cause these flare-ups. The common triggers include certain foods, change in weather, stress, and certain hair products. Reduce the use of hair styling products as they can irritate your scalp. Also, keep your hair clean to prevent scalp build-up as it can worsen your hair care issues.

  • Natural remedies

    Tea tree oil, olive oil, and aloe vera are some of the common home remedies used to treat dandruff and scalp eczema. However, these remedies only offer temporary relief from the incessant scratching. You’ll need something stronger to prevent flaking and inflammation.

Consult a doctor if the condition worsens or your scalp appears infected. The symptoms of infection include:

• White or yellow pus
• Blistered skin
• Severe itchiness
• New burning sensations
• Fluid drainage

Scalp eczema cannot be fully treated, but you can keep the condition in check with the help of these tips and products from Head & Shoulders.

How To Tell The Difference

If your scalp itches and flakes, your doctor can tell if it’s just dandruff or a more serious problem like psoriasis, a disease that causes red, scaly patches on your skin. Once you have the right diagnosis, you can treat the cause and get some relief.

What Is Dandruff?

Dandruff is a common skin problem. You may notice flakes that fall off your scalp and cling to your hair or land on your clothing. Your scalp may itch, too.

Several things can cause dandruff:

  • Seborrheic dermatitis: This is oily, itchy, irritated skin that flakes off on your scalp. It also can happen with your eyebrows, groin, or chest hair.
  • Contact dermatitis: Hair care products like shampoo, gel, or dye can irritate your scalp and cause redness, itchiness, and flakes.
  • Fungus called malassezia is a yeast that thrives on the oil on your scalp.
  • If you don’t shampoo your hair often enough, oily skin can flake off.
  • Dry skin can lead to small flakes on your scalp. You’ll probably have dry skin all over your body.
  • Male hormones:Men are more likely to get dandruff than women.
  • People whose immune systems can’t fight off diseases, for instance people who have HIV, may be more likely to get dandruff.

Dandruff usually isn’t serious. You can’t catch it from anyone else or pass it on. It can be uncomfortable or embarrassing, though. Dandruff can be treated at home without a prescription.

What Is Scalp Psoriasis?

Psoriasis can affect your scalp, and the red, scaly patches it causes can flake off like dandruff does. There are a few differences, though:

  • It’s chronic: Psoriasis is long-lasting while dandruff may come and go.
  • It’s more scaly than flaky. If it’s mild, scalp psoriasis looks like scaly, silvery, or powdery patches that may come off in tiny pieces. More serious outbreaks can be red and painful.
  • It may spread. Psoriasis patches can creep past your hairline to your forehead, the back of your neck, or the skin around your ears. You may have psoriasis patches on other parts of your body, too, like your elbows, legs, feet, palms, or back.
  • It’s an autoimmune disease. Psoriasis is caused by your body’s immune system: White blood cells that should fight off diseases attack your skin cells instead.

View a slideshow to see what scalp psoriasis looks like.

 

Diagnosis

Your doctor may figure out the reason your scalp flakes or itches just from your symptoms. To be sure, they may look at a small piece of skin from your scalp under a microscope or send it to a lab.

Treatment

If you have mild dandruff because your scalp is greasy or oily, you may just try a regular, gentle shampoo.

If that doesn’t help, some shampoos are made to control dandruff. They may have zinc pyrithione (Head & Shoulders, Free & Clear), coal tar (Neutrogena T/Gel), salicylic acid (Neutrogena T/Sal), selenium sulfide (Selsun Blue), or ketoconazole (Nizoral). Tea tree oil is an alternative treatment for dandruff. Follow the directions on the shampoo bottle.

Your doctor or pharmacist can point you to the right shampoo for you. You also can get a prescription dandruff product if over-the-counter shampoos don’t stop your itch and flakes.

Coal tar and salicylic acid shampoos or scalp treatments may also help with mild scalp psoriasis.

Topical creams, ointments, and foams like the following can slow psoriasis skin buildup and ease red, scaly patches on your scalp. They may have vitamins or steroids to calm the inflammation:

  • Anthralin (Zithranol-RR)
  • Calcipotriene (Dovonex)
  • Calcipotriene and betamethasone dipropionate (Taclonex)
  • Calcitriol (Vectical)
  • Tazarotene (Tazorac)

Your doctor can also put steroids (strong anti-inflammatory drugs) into the patches on your scalp if your psoriasis is milder or just in a few spots. If you have severe psoriasis, you may need stronger drugs. These include methotrexate, which affects how certain cells grow; cyclosporine, which slows down your immune system; biologics, which target specific areas of your immune system; or oral retinoids, which are high doses of vitamin A.

You can also try ultraviolet or UV light treatments to control your psoriasis patches. You can part your hair in rows so UV light from a special lamp can reach your scalp or use a handheld UV comb that beams the light directly to your scalp.

Dandruff (for Teens) – Nemours Kidshealth

What Is Dandruff?

Dandruff is a common scalp condition that that causes flaky skin and an itchy scalp. 

What Are the Signs & Symptoms of Dandruff?

Common signs and symptoms of dandruff include:

  • white flakes of dead skin in your hair and on your shoulders
  • red, crusty, or raw areas on your scalp
  • an itchy scalp

What Causes Dandruff?

Dandruff is a mild form of seborrheic dermatitis. The exact cause of seborrheic dermatitis is not known, but it’s likely a combination of things like:

  • too much skin oil (sebum) in the oil glands and hair follicles
  • a type of yeast found on the skin called Malassezia

Stress, cold and dry winter weather, and some hair care products may make dandruff worse.

Almost anyone can have dandruff. Many teens and adults live with it. Hormone levels are high during teen years, which causes more oil production. This may be why dandruff usually begins around puberty.

Dandruff isn’t contagious. You can’t catch it from or give it to another person.

How Is Dandruff Diagnosed?

Health care providers can diagnose dandruff and seborrheic dermatitis based on symptoms (like an itchy scalp and flakes on the shoulders) and an exam.

How Is Dandruff Treated?

In most cases, over-the-counter dandruff shampoo can control a person’s dandruff. Check the labels for these common “active ingredients”:

  • selenium sulfide 1% shampoo (such as Selsun Blue®, or a store brand)
  • zinc pyrithione shampoo (such as Head & Shoulders®, Zincon®, DHS zinc®, or a store brand)
  • tar-based shampoo (such as T-Gel®, DHS tar®, Pentrax®, or a store brand). Tar-based shampoos can make the scalp more sensitive to sunlight, so users should wear a hat outside. Don’t use a tar shampoo on dyed or treated hair. Long-term use can stain skin, hair, and nails.
  • ketoconazole shampoo (such as Nizoral 1%® or a store brand)

Follow the label directions on how much to use and how often. When your dandruff improves, it’s OK to use dandruff shampoo less often. Once a week might be enough to keep flakes off your shoulders.

If dandruff doesn’t get better after 4–6 weeks, try another shampoo with a different active ingredient.

Talk to the pharmacist if you have any questions about dandruff shampoos.

When Should I Call the Doctor?

Call your health care provider if:

  • Your dandruff doesn’t go away with dandruff shampoo.
  • Dandruff or itching gets worse.
  • Your scalp gets red or swollen.
  • You have red and flaky skin in areas other than your scalp.

The doctor may prescribe prescription-strength shampoos or topical steroids for itching and redness.

What Else Should I Know?

People with dandruff also may get seborrheic dermatitis on other parts of their body, including:

  • eyebrows
  • nose creases
  • behind the ears
  • in sideburns and beard areas

Do You Have Dandruff Or Is It Seborrheic Dermatitis?: Northstar Dermatology: Dermatology

More Than Dandruff?

Read Time: 3 minutes

Dandruff is a common condition that will affect at least 1 in 2 persons in their lifetime. The small white flakes and irritation can shatter self-esteem and cost thousands in yearly treatment. Sometimes, people confuse dandruff for a condition called seborrheic dermatitis. By observing key differences, persons can tell which is affecting them and get the right treatment.

The case of unwanted flakes

With dandruff, small pieces of dead skin flake off and appear in the head and on the shoulders. The body naturally sheds skin every second. These skin cells are invisible. However, in some people, these skin cells appear larger on the scalp. The flakes can seem unsightly and often has some social stigma attached to the issue. Besides flakes, persons with dandruff experience a dry, itchy scalp.

What causes the condition?

The real cause of dandruff is still unknown. Many people incorrectly point to poor hygiene as the main cause. Not shampooing enough will cause dandruff to appear more; However, hygiene is not the main reason. Other causes include harsh hair products, stress, and a poor diet. Researchers also attribute dandruff to the Malassezia fungus. The fungus interacts with the oils on the scalp which can cause an overreaction in some cases. The cause of this reaction could even be genetic. Persons with dandruff should seek help from a dermatologist.

A deeper condition than dandruff

Sometimes, what one assumes is dandruff can be seborrheic dermatitis. This condition affects about 1 in 3 persons worldwide. If dandruff is a mild reaction, seborrheic dermatitis is an extreme case. The inflammation worsens, causing harsh redness, flakiness, and a scaly scalp. Also, seborrheic dermatitis can happen anywhere on the body that has sebaceous glands. This includes the nose, mouth, back, and shoulders. There are even cases of seborrheic dermatitis under the armpits, ears, or chest area. The condition impacts the quality of life and needs medical help to manage.

Causes of seborrheic dermatitis

Similar to dandruff, seborrheic dermatitis is a harsh reaction to fungi that naturally lives on all humans. This is common in infants and referred to as a cradle cap. Whereas in adults, stress, hormonal changes, and dry weather can cause flare-ups. Diseases like Parkinson’s, psoriasis and HIV can cause seborrheic dermatitis.

Which one do you have?

Unsure if the issue is dandruff or seborrheic dermatitis? Check for simple signs. Dandruff will appear as white, oily flakes at the root of the scalp. In most cases, dandruff may not cause itching. So a pharmacist can prescribe a medicated shampoo. However, if the flakes come with scaly patches on the scalp, this could be a sign of seborrheic dermatitis. Red patches around the nose and oily, tender skin are other early signs. Some cases may need stronger treatment like a corticosteroid. Seek help immediately if these symptoms pop up.

Get help today

Both conditions can be treated with help from a medical professional. While both have similar symptoms, dandruff and seborrheic dermatitis differ in damage to the head and body. Know of the signs to know which one is the issue. There’s no known cure for both conditions. Dandruff and seborrheic dermatitis can impact persons socially. Using the right treatment reduces symptoms, keeping persons healthy and happy.

Seborrheic Dermatitis and Dandruff: A Comprehensive Review

J Clin Investig Dermatol. Author manuscript; available in PMC 2016 May 2.

Published in final edited form as:

J Clin Investig Dermatol. 2015 Dec; 3(2): 10.13188/2373-1044.1000019.

Published online 2015 Dec 15. doi: 10.13188/2373-1044.1000019

PMCID: PMC4852869

NIHMSID: NIHMS754376

Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, 1600 NW 10th Avenue, RMSB 2023A, Miami, Florida 33136, USA

*Address for Correspondence. Tongyu C. Wikramanayake, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, 1600 NW 10th Avenue, RMSB 2023A, Miami, Florida 33136, USA, Tel: (305) 243-8878; Fax: (305) 243-3082; ude. [email protected]

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

See other articles in PMC that cite the published article.

Abstract

Seborrheic Dermatitis (SD) and dandruff are of a continuous spectrum of the same disease that affects the seborrheic areas of the body. Dandruff is restricted to the scalp, and involves itchy, flaking skin without visible inflammation. SD can affect the scalp as well as other seborrheic areas, and involves itchy and flaking or scaling skin, inflammation and pruritus. Various intrinsic and environmental factors, such as sebaceous secretions, skin surface fungal colonization, individual susceptibility, and interactions between these factors, all contribute to the pathogenesis of SD and dandruff. In this review, we summarize the current knowledge on SD and dandruff, including epidemiology, burden of disease, clinical presentations and diagnosis, treatment, genetic studies in humans and animal models, and predisposing factors. Genetic and biochemical studies and investigations in animal models provide further insight on the pathophysiology and strategies for better treatment.

Keywords: Seborrheic dermatitis, Dandruff, Sebaceous gland, Malassezia, Epidermal barrier

Introduction

Seborrheic Dermatitis (SD) and dandruff are common dermatological problems that affect the seborrheic areas of the body. They are considered the same basic condition sharing many features and responding to similar treatments, differing only in locality and severity. Dandruff is restricted to the scalp, and involves itchy, flaking skin without visible inflammation. SD affects the scalp as well as face, retro-auricular area, and the upper chest, causing flaking, scaling, inflammation and pruritus, and can have marked erythema. Flaking in SD and dandruff is usually white-to-yellowish, and may be oily or dry.

It is estimated that SD and dandruff combined affect half of the adult population. Despite such high prevalence, their etiology is not well understood. Various intrinsic and environmental factors, such as sebaceous secretions, skin surface fungal colonization, individual susceptibility, and interactions between these factors, all contribute to the pathogenesis. Genetic, biochemical studies and investigations in animal models further provided insight on the pathophysiology and strategies for better treatment. In this comprehensive review, we summarize the current knowledge on SD and dandruff, and attempt to provide directions for future investigations and treatments.

Epidemiology

SD is a common dermatological disorder in the United States and worldwide [1]. Its incidence peaks during three age periods – in the first three months of life, during puberty, and in adulthood with an apex at 40 to 60 years of age [1–4]. In infants up to three months of age, SD involves the scalp (termed “cradle cap”), the face, and diaper area. Incidence can be up to 42% [4–6]. In adolescents and adults, SD affects the scalp and other seborrheic areas on the face, upper-chest, axillae, and inguinal folds [4,7,8]. Incidence is 1–3% of the general adult population [3,9]. Men are affected more frequently than women (3.0% vs. 2.6%) in all age groups, suggesting that SD may be associated with sex hormones such as androgens [1,3,8]. No apparent differences were observed in SD incidence between ethnic groups [3].

SD is more prevalent in immune-compromised patients such as HIV/AIDS patients [7,10], organ transplant recipients [11,12], and patients with lymphoma [13]. The incidence among HIV patients ranges from 30% to 83% [9,10]. Most cases of SD in HIV patients are diagnosed with CD4+ T lymphocyte counts between 200 and 500/mm3 [3,14,15], and decreased CD4+ counts are often associated with worse SD. Fewer cases of SD were reported when CD4+ T cells were more than 500/mm3 [14]. These observations suggest that immunological defects may play a role in SD.

SD is also associated with neurological disorders and psychiatric diseases, including Parkinson’s disease, neuroleptic induced parkinsonism, tardive dyskinesia, traumatic brain injury, epilepsy, facial nerve palsy, spinal cord injury and mood depression [4,5,16,17], chronic alcoholic pancreatitis, hepatitis C virus [18,19], and in patients with congenital disorders such as Down syndrome [20]. Furthermore, seborrhea-like dermatitis of the face may also develop in patients treated for psoriasis with psoralen and ultraviolet A (PUVA) therapy [21].

Comparing with SD, dandruff is much more common, and affects approximately 50% of the general adult population worldwide. It is also more prevalent in males than females [22,23]. Dandruff starts at puberty, reaches peak incidence and severity at the age of about 20 years, and becomes less prevalent among people over 50 [23]. Incidence varies between different ethnic groups: in a study in the U.S. and China, dandruff prevalence was 81–95% in African Americans, 66–82% in Caucasians, and 30–42% in Chinese [23].

Burden of Disease

It is estimated that at least 50 million Americans suffer from dandruff, who spend $300 million annually on over-the-counter products to treat scalp itching and flaking [22]. Besides physical discomfort such as itching, dandruff is socially embarrassing and negatively impacts patients’ self-esteem [22].

While SD is much less prevalent, outpatient office visits alone cost $58 million in the United States in 2004, and $109 million were spent on prescription drugs [24]. Together with over-the-counter products and hospital services, the total direct costs of SD were estimated to be $179 million, plus another $51 million indirect costs in the form of lost work days [24]. In addition, because SD frequently occurs on the face and other visible areas, it has significant negative effects on patients’ quality of life (QOL) in the form of psychological distress or low self esteem; the willingness to pay for relief of the symptoms was $1.2 billion [24]. Furthermore, although the QOL impact in SD patients ranked lower than in patients with atopic or contact dermatitis, it was found to be higher than skin ulcers and solar radiation damage, and women, younger patients, and subjects with higher educational level were more affected [24].

Clinical Presentation and Diagnosis

Clinical presentations

The clinical presentations of SD and dandruff in children and adults are summarized in . SD often presents as well-delimited erythematous plaques with greasy-looking, yellowish scales of varying extents in regions rich in sebaceous glands, such as the scalp, the retro-auricular area, face (nasolabial folds, upper lip, eyelids and eyebrows), and the upper chest. Distribution of the lesions is generally symmetrical, and SD is neither contagious nor fatal. SD has a seasonal pattern, presenting more frequently during winter, and improving usually during summer [5,25,26]. Additionally, aggravation of SD has been associated with sleep deprivation and stress [7,27,28].

Table 1

Clinical presentations of seborrheic dermatitis (SD) and dandruff.

Features
Dandruff Light, white to yellow and dispersed flaking on the scalp and hair without erythema. Absent to mild pruritus. Can spread to hairline, retro-auricular area and eyebrows.
SD in Infants Scalp Cradle Cap: Most Common. Red-yellow plaques coated by thick, greasy scales on vertex, appearing within 3 months of age.
Face/Retro-auricular area Erythematous, flaky, salmon-colored plaques on forehead, eyebrows, eyelids, nasolabial folds, or retro-auricular areas.
Body folds Lesions have moist, shiny, non-scaly aspects that tend to coalesce on neck, axillae or inguinal area.
Trunk More extensive form: Sharply limited plaques of erythema and scaling that cover lower abdomen.
Generalized Leiner’s Disease: Unusual, associated with immunodeficiency. Absent to mild pruritus. Concurrent diarrhea and failure to thrive. Spontaneous clearing within weeks to few months.
SD in Adults Scalp From mild desquamation to honey-colored crusts attached to scalp and hair leading to alopecia. May reach into forehead as scaly erythematous border known as “corona seborrheica”.
Face/Retro-auricular area Forehead, eyebrows, glabella or nasolabial folds. May spread to malar regions and cheeks in butterfly distribution.
Eyelids: Yellowish scaling between eye lashes. Can lead to blepharitis with honey-colored crusts on free margin.
Retro-auricular area: Crusting, oozing and fissures. May expand to external canal, with marked itching on occasionally secondary infection (otitis externa).
Upper Chest Petaloid type (common): small, reddish follicular and peri-follicular papules with oily scales at onset that become patches resembling a medallion (flower petals).
Pityriasiform type: Widespread 5–15 mm oval-shaped, scaly macules and patches. Distributed along the skin tension lines (similar to extensive pityriasis rosea). New eruptions can continue for >3 months. Commonly on face and intertriginous areas.
Body Folds Moist, macerated appearance with erythema at the base and periphery on axillae, umbilicus, breast fold, genital or inguinal area. May progress to fissures and secondary infection.
SD with immune-suppression* Extensive, severe and refractory to treatment. In both children and adults with AIDS†. Unusual sites involved such as extremities. More widespread with CD4 counts <200 cells/mm3. Associated with rosacea, psoriasis and acne.

In infants, SD may present on the scalp, face, retro-auricular area, body folds, and trunk; rarely it may be generalized. Cradle cap is the most common clinical manifestation. SD in children is usually self-limited [3,15]. On the other hand, in adults, SD is a chronic or relapsing condition, featured by erythematous patches, with flaky, large, oily or dry scales in sebum-rich areas such as face (87. 7%), scalp (70.3%), upper trunk (26.8%), lower extremities (2.3%), and upper extremities (1.3%) [5,7,29]. Pruritus is not an obligatory feature, but it is often present, mainly in scalp involvement [2]. The main complication is secondary bacterial infection, which increases the redness and exudate and local irritation [3,15].

In immune-suppressed patients, SD is often more extensive, intense, and refractory to treatment [3,26,30]. It is considered an early skin presentation of AIDS in both children and adults [14]. SD may also be a cutaneous sign of the immune reconstitution inflammatory syndrome in patients with highly active antiretroviral therapy (HAART) [31]. However, there have also been reports of SD regression with HAART [10].

Differential diagnosis

The main differential diagnosis of SD and dandruff includes psoriasis, atopic dermatitis (mainly in the pediatric form of SD), tinea capitis, rosacea, and systemic lupus erythematous (SLE) [3,7,8] (). While psoriasis can affect similar locations as SD, typical lesions in psoriasis are thicker and present as plaques sharply limited with silvery white scales [8,32]. Lesions in atopic dermatitis usually do not appear until after 3 months of age, while lesions in SD usually appear earlier and rarely affect extensor areas. Tinea capitis, a highly contagious disease, typically shows scaly patches of scalp hair loss associated with “black dots”, which represent distal ends of broken hairs [33]. Conversely, SD is not associated with hair loss. Rosacea usually targets the malar areas on the face, sparing the nasolabial folds, and do not have scales; on the other hand, facial SD lesions are usually scaly, and affect the nasolabial folds, eyelids, and eyebrows, without associated flushing or telangiectasias [7,8,34]. Finally, skin lesions in SLE often follow a clear photo distribution, such as acute flares of bilateral malar rash, and may be associated with extra-cutaneous abnormalities such as arthritis, mouth ulcers, glomerulonephritis or cardiomyopathy [8,35]; SD does not have a photo distribution pattern, and does not affect organ systems other than the skin.

Table 2

Differential diagnosis of seborrheic dermatitis and dandruff.

Diagnosis Diagnostic Clues
Psoriasis Usually involves extensor, palmar, plantar, nails and extensor areas. Thick plaques sharply limited with silvery white scales. Positive family history. Arthritis present in 10% of patients. Uncommon in children.
Atopic Dermatitis First appearance after 3 months of age, pruritus and restlessness are common. Frequently involves scalp, cheeks and extensor areas. Flexures involvement is more frequent in older ages. Family history of atopy such as eczema, allergic rhinitis and asthma. Self resolved by age 12.
Tinea Capitis Commonly seen in children, frequently accompanied by hair loss patches with “black dots” (broken hair). Highly contagious. KOH examination of the hair shaft and fungal culture confirm the diagnosis. Household members of patient should be examined.
Rosacea Usually targets the face. Papulopustules and telangiectasias on the malar, nose and perioral regions with slight desquamation. Recurrent edema and flushing.
Systemic Lupus Erythematous (SLE) In acute stage, butterfly rash on face that spares the nose bridge or nasolabial folds. Photosensitivity is common. Skin lesions are generally associated with other clinical signs of SLE. Histology and serologic tests such as antinuclear autoantibodies confirm the diagnosis.
Others Pemphigus Foliaceous Erythema, scaling and crusting that first present on the scalp and face can expand to chest and back. Histology, direct immunofluorescence with anti-desmoglein antibodies confirm diagnosis.
Pityriasis Rosea Abrupt onset, appearance of herald patch and resolution within weeks.
Secondary syphilis Peripheral lymph-adenopathy, mucosal lesions and palmoplantar macula-papules. Serology tests such as VDRL/ RPR, FTA-ABS* confirm diagnosis.
Diaper Dermatitis Occurs on convex skin surfaces in contact with diaper, such as lower abdomen, genitalia, buttocks and upper thighs. Spares skin folds. Pustules are common.
Langerhans cell histiocytosis Multisystem disease. Brown to purplish papules prone to coalesce on the scalp, retro-auricular areas, axillae and inguinal folds. Possible lytic bone lesions, liver, spleen and lung involvement. Histology confirms diagnosis.

Other less common conditions that may resemble SD are pemphigus foliaceous, pityriasis rosea, secondary syphilis, diaper dermatitis and cutaneous Langerhans cell histiocytosis [3,4,7,30], which are summarized in . The majority of these conditions can be differentiated by clinical presentation and history; although syphilis, pemphigus foliaceous and SLE may require laboratory confirmation.

Additionally, some drugs (griseofulvin, ethionamide, buspirone, haloperidol, chlorpromazine, IL-2, interferon-α, methyldopa, psoralens) and nutritional deficiencies (pyridoxine, zinc, niacin and riboflavin) may induce an SD-like dermatitis, although the mechanism remains unknown [36,37]. These conditions can coexist with SD as well, making the diagnosis more challenging.

Pathology

Diagnosis of SD is typically made by history and physical examination. In rare cases, a skin biopsy is needed for differential diagnosis. Histologically, the development of SD can be divided into two stages. In the acute and sub-acute stages, SD shows superficial perivascular and perifollicular inflammatory infiltrates, composed mainly of lymphocytes and histiocytes in association with spongiosis and psoriasiform hyperplasia, and can be coupled with parakeratosis around follicular opening (“shoulder parakeratosis”). Neutrophils can also be found in the scale crust at the margins of follicular ostia. On the other hand, in chronic lesions, marked psoriasiform hyperplasia and parakeratosis can be present with dilation of the venules of surface plexus which resembles psoriasis [3,4,38]. However, in psoriasis parakeratosis is often associated with thinning or loss of the granular layer due to accelerated keratinocyte differentiation.

Dandruff shows many common features as SD in histology, such as epidermal hyperplasia, parakeratosis, and Malassezia yeasts surrounding the parakeratotic cells [23]. Whereas inflammatory cells such as lymphocytes and NK cells may be present in great numbers in SD, dandruff shows subtle neutrophil infiltration or no infiltration. These findings support the notion that dandruff and SD are of a continuous spectrum of the same disease entity with different severity and location [39].

Treatment

Treatment of SD and dandruff focuses on clearing signs of the disease; ameliorating associated symptoms, especially pruritus; and maintaining remission with long-term therapy. Because the main underlying pathogenic mechanisms involve Malassezia proliferation and local skin irritation and inflammation, the most common treatment is topical antifungal and anti-inflammatory agents (). Other widely used therapies are coal tar, lithium gluconate/ succinate and phototherapy (). New therapies have also emerged including immune modulators such as topical calcineurin inhibitors, and metronidazole, but their efficacy remains controversial [5]. Alternative therapies have been reported as well, such as tea tree oil [40,41]. Some factors to be considered before selecting a treatment include efficacy, side effects, ease of use/compliance, and age of the patient [5]. Systemic therapy is needed only in widespread lesions and in cases that do not respond to topical treatment [3,26].

Table 3

Treatment of seborrheic dermatitis and dandruff.

Medication Dose/
Formulation
Regimen Mechanisms Side Effects References
TOPICAL Antifungals Ketoconazole 2% Shampoo, cream, gel or foam Scalp or skin: Twice/week × 4 weeks, then once/week for maintenance. Inhibition of fungal cell wall synthesis. ICD in <1% of patients. Itching, burning sensation and dryness in 3% of patients. [2,8,26,97–101]
Bifonazole 1% shampoo, cream or ointment Scalp: every other day or once daily.
Skin: once daily.
ICD in 10% of patients. [8,26,99,102]
Miconazole Cream Skin: 1–2 times daily. ICD, itching, burning sensation. [47,97,103]
Ciclopirox Olamine 1.5% shampoo, cream, gel or lotion Scalp: 2–3 times/week × 4 weeks, then once/week for maintenance.
Skin: twice daily.
Inhibition of metal-dependent enzymes. ICD in <1% of patients. Itching, burning sensation in 2% of patients. [8,47,97,99,104,105]
Selenium sulfide 2.5% shampoo Scalp: Twice/week × 2 weeks, then once/week × 2 weeks. Repeat after 4–6 weeks. Cytostatic and keratolytic. ICD in ~3% of patients. Orange-brown scalp discoloration. [8,97,106,107]
Zinc Pyrithione 1% shampoo Scalp: 2–3 times/week. Increased cellular copper interferes with iron-sulfur proteins. ICD in ~3% of patients. [8,97,99,101,108,109]
Cortico-steroids Hydrocortisone 1% cream Skin: 1–2 times daily. Anti-inflammatory, anti-irritant. Risk of skin atrophy, telangiectasias, folliculitis, hypertrichosis, and hypopigmentation with prolonged use. [8,9,97,99,103,108]
Betamethasone dipropionate 0.05% lotion Scalp and skin: 1–2 times daily. [8,47,110]
Desonide 0.05% lotion, gel Scalp and skin: 2 times daily. [8,111–113]
Fluocinolone 0.01% shampoo, lotion or cream Scalp or skin: Once or twice daily. [7,114]
Immuno-modulators Pimecrolimus 1% cream Skin: 1–2 times daily. Inhibition of cytokine production by T-lymphocyte. Risk of skin malignancy and lymphoma with prolonged use. [47,98,115–118]
Tacrolimus 0.1% ointment Skin: 1–2 times daily × 4 weeks, then twice/week for maintenance. [26,97,109,118–120]
Miscellaneous Coal tar 4% shampoo Scalp: 1–2 times/week. Antifungal, anti-inflammatory, keratolytic, reduces sebum production. Local folliculitis, ICD on fingers, psoriasis aggravation, skin atrophy, telangiectasias, hyper-pigmentation. Risk of squamous cell carcinoma with prolonged use. [4,8,47,117,121]
Lithium gluconate/succinate 8% ointment or gel Skin: twice daily × 8 weeks. Anti-inflammatory via increased IL-10 and decreased TLR2 and TLR4 in keratinocytes. ICD in <10% of patients. [8,122–124]
Metronidazole 0.75% gel Skin: twice daily × 4 weeks. Anti-inflammatory via inhibition of free radical species. Rare contact sensitization with prolonged use. [5,47,125,126]
Phototherapy UVB: Cumulative dose of 9.8 J/cm2 Three time/week × 8 weeks or until clearing. Immuno-modulation and inhibition of cell proliferation. Burning, itching sensation during/after therapy. Risk of genital tumor with prolonged use. [26,127–129]
SYSTEMIC Itraconazole Oral: 200 mg Once daily × 7 days, then once daily × 2 days/month for maintenance. Inhibition of fungal cell wall synthesis. Anti-inflammatory via inhibition of 5-lipoxygenase metabolites. Rare liver toxicity. [97,130,131]
Terbinafine Oral: 250 mg Once daily × 4–6 weeks or 12 days monthly × 3 months. Inhibition of cell membrane and cell wall synthesis. Rare tachycardia and insomnia. [132–134]

Pathophysiology

Despite the high prevalence, the pathogenesis of SD and dandruff is not well understood. However, studies have identified several predisposing factors, including fungal colonization, sebaceous gland activity, as well as several factors that confer individual susceptibility [2].

Fungal colonization

Several lines of evidence suggest a pathogenic role for yeasts of the genus Malassezia in SD and dandruff [42–46]. Malassezia are lipophilic yeasts that are found mainly on seborrheic regions of the body [5,7,47]. Studies have detected Malassezia on the scalp of dandruff patients [45,48], and higher numbers of Malassezia (M. globosa and M. restricta) correlate with SD appearance/severity [4,49,50]. Additionally, among the multiple chemical entities that are effective in treating SD and dandruff, such as azoles, hydroxypyridones, allylamines, selenium and zinc, the sole common mechanism of action is antifungal activity [47–49]. Furthermore, Malassezia was shown to have lipase activity, which hydrolyzes human sebum triglycerides and releases unsaturated fatty acids such as oleic and arachidonic acid [51,52]. These metabolites cause aberrant keratinocytes differentiation, resulting in stratum corneum abnormalities such as parakeratosis, intracellular lipid droplets, and irregular corneocyte envelope [53]. Such changes lead to disrupted epidermal barrier function and trigger inflammatory response, with or without visible local inflammation. In addition, these metabolites induce keratinocytes to produce pro-inflammatory cytokines such as IL-1α, IL-6, IL-8 and TNF-α, thus prolonging the inflammatory response [39,54]. Furthermore, arachidonic acid can be a source of prostaglandins, which are pro-inflammatory mediators that can cause inflammation via neutrophil recruitment and vasodilation [38]. Interestingly, Malassezia infection has also been reported in goats, dogs and monkeys with seborrhea (dry or greasy) and dermatitis [55– 59].

While these observations support a pathogenic role for Malassezia in SD and dandruff, there is also strong evidence suggesting that individual predispositions and host interactions with Malassezia, rather than the mere presence of Malassezia, contribute to SD and dandruff pathogenesis. For example, Malassezia was detected on normal skin of majority of healthy adults, making it a commensal organism [2,5,26]. Moreover, while topical application of oleic acid did not induce visible changes in non-dandruff subjects, it caused skin flaking on the non-lesional scalp of dandruff patients [48]. These observations are suggestive of intrinsic epidermal barrier defects in the pathogenesis of SD and dandruff [48].

Sebaceous gland activity

Sebaceous glands (SGs) are distributed over the entire skin surface in humans, except on the palms and soles. Secretion of sebum is highest on the scalp, face and chest [44]. Sebum production is under hormonal control, and SGs are activated at birth under the influence of maternal androgens via androgen receptors in sebocytes [60]. SGs are activated again at puberty under the control of circulating androgens [38,61], resulting in increased sebum secretion during adolescence, which is kept stable between 20 and 30 years of age and is then reduced [62]. During the period of active sebum secretion, the secretion rate is higher in males and stays high longer, between 30 and 60 years of age; in females, the rate drops fast after menopause [44]. Thus, SD and dandruff have a strong time correlation with SG activity, with cradle cap after birth, increased incidence throughout the teens, between third and sixth decades and then decreasing [3,4,9]. However, SD patients may have normal sebum production, and individuals with excessive sebum production sometimes don’t develop SD [38,63]. These findings suggest that while SG activity strongly correlates with SD and dandruff, sebum production by itself is not a decisive cause.

In addition to the level of sebum production, abnormalities of lipid composition may also play a role in SD development, likely through a favorable milieu for Malassezia growth [64]. In patients with SD, triglycerides and squalene were reduced, but free fatty acids and cholesterol were considerably elevated [38,44]. The elevated levels of free fatty acids and cholesterol may be the result of triglyceride degradation by Malassezia’s lipase, and these metabolites promote Malassezia growth and lead to recruitment of inflammatory infiltrates in the skin [64].

Individual susceptibility

Besides sebaceous activity and Malassezia colonization, other factors also contribute to the pathogenesis of SD. Epidermal barrier integrity, host immune response, neurogenic factors and emotional stress, and nutritional factors have all been shown to play a role in individual susceptibility.

Epidermal barrier integrity

The stratum corneum (SC), the anucleated outer layers of the epidermis, functions as a barrier against water loss and entry of microorganisms and harmful agents from the environment [65]. The SC consists of several layers of terminally differentiated keratinocytes, the “corneocytes”, encased in lipid lamellae, held together by specialized intercellular cell adhesion structures called corneodesmosomes [66]. Any changes in the lamellar lipid composition, corneocyte size or shape, corneodesmosome number and SC thickness, could lead to alterations in the epidermal permeability barrier (EPB) function [66].

Normally, sebum may influence intercellular lipid organization to aid desquamation [66,67]. In SD and dandruff, however, altered corneodesmosomal hydrolysis may disrupt lipid organization and disturb the desquamation process, leading to aberrant barrier function [53,68]. In support of this notion, barrier structural abnormalities have been detected in dandruff scalp by electron microscopy that included intercellular Malassezia yeasts, changes in corneocyte shape and corneodesmosomes, and disrupted lipid lamellar structure [23,53,66]. Consistent with the structural findings, dandruff patients have been found to be more reactive (higher itch perception or flaking) than controls to topical applications of histamine or oleic acid to the scalp [48,69,70]. These observations indicate that disrupted EPB function can contribute to the aggravation of dandruff. Recent genetic studies in humans and animals suggest that disrupted barrier function may even directly cause SD-like conditions [71]. Biochemical analysis further demonstrated that dandruff skin displayed altered protein profiles as well as those of SC ceramides and free fatty acids, in the absence of apparent inflammation [72]. These studies underscore the importance of barrier restoration and maintenance in the management of SD and dandruff.

Immune response

Both the incidence and severity of SD are associated with immune-suppression, particularly in HIV/AIDS patients. Because no clear differences were found in Malassezia levels between individuals with and without SD in this population, it is likely that an immune or inflammatory reaction could be the predisposition [5,9]. Indeed, one study found elevated levels of human leukocyte antigens HLA-AW30, HLA-AW31, HLA-A32, HLA-B12 and HLA-B18 in SD [3,73,74]. Additionally, increased levels of total serum IgA and IgG antibodies have been detected in SD patients [75]. However, no increase in the titers of antibodies against Malassezia was detected, suggesting that the elevated immunoglobulin production occurs rather as a response to yeast metabolites [26,75,76]. The strong inflammatory reaction provoked by these metabolites includes infiltration of Natural Killer (NK) cells and macrophages, with concurrent local activation of complement and an increased local production of inflammatory cytokines, such as IL-1α, IL-1β, IL-6 and TNF-α in affected skin areas [54]. The lack of increase in anti-Malassezia antibodies also indicates a change in cellular immune response instead of humoral response [76,77]. The specific role of lymphocyte activity remains controversial [76–79].

Genetic factors

The genetic components of SD and dandruff had been under-appreciated until recently, when studies in animal models and humans identified inherited dominant and recessive forms of SD and dandruff. In the autosomal recessive “inherited seborrheic dermatitis” (seb) mice, a spontaneous mutation in the outbred Him:OF1 mice caused seborrhea, rough coat, alopecia, growth retardation, and sometimes abnormal pigmentation in homozygous mutants [80]. Histological examination revealed enlarged sebaceous glands, hyperkeratosis, parakeratosis, acanthosis and inflammatory infiltrates in the epidermis and dermis. Neither yeasts nor dermatophytes were detected. These mice were the first animal model of SD to show a clear mode of inheritance, though the underlying mutation remains unidentified [80,81].

Consistent with a role for altered immunity in the pathogenesis of SD, transgenic mice carrying the 2C T cell receptor (TCR) transgene in the DBA/2 background developed extremely inflammatory phenotype in seborrheic areas, such as the ears, around the eyes, and muzzle area [82]. Additionally, positive fungal staining by PAS was consistently detected in lesional skin but not readily apparent in non-lesional skin from diseased mice or from DBA/2 control mice. Furthermore, antifungal treatment reversed clinical and pathology presentations, and reduced PAS staining [82]. These observations support the notion that immune compromise and fungal infection play active roles in SD.

Another spontaneous mutant mouse strain that shows SD-like phenotype is the rough coat (rc) mice, which showed sebaceous hypertrophy and greasy hair coat, alopecia, and growth retardation [83]. The rc is transmitted in an autosomal recessive mode. We have since identified the cause of the rc phenotype to be a missense mutation in the Mpzl3 gene, which is expressed in the superficial layers of the epidermis [84,85]. Our Mpzl3 knockout mice recapitulated the rc phenotype, and mice with white hair coat developed more severe and persistent inflammatory skin phenotype and dandruff in the seborrheic areas [85]. We have shown that the early-onset inflammatory skin phenotype was not caused by immune defects [85]. However, skin abnormalities in Mpzl3 knockout mice and perturbed epidermal differentiation in organotypic human skin models with MPZL3 knockdown indicate that MPZL3 is a key regulator of epidermal differentiation [85,86]. Interestingly, a frame-shift mutation in ZNF750, a transcription factor controlling epidermal differentiation and an upstream regulator of MPZL3, caused autosomal dominant seborrhea-like dermatitis in patients [71,86]. These studies in humans and animal models underscore the consequence of abnormal epidermal differentiation in the pathogenesis of SD and dandruff, and have provided the genetic basis for some of the predisposing factors discussed above. These animal models will be important tools to dissect the underlying pathways that will identify novel targets for better treatment of these disorders.

Neurogenic factors and emotional stress

The high incidence of SD in patients with Parkinson’s disease [17,87,88] and neuroleptic-induced Parkinsonism [89,90] has long been observed, especially in those with severe seborrhea, which provides favorable conditions for Malassezia proliferation. Bilateral seborrhea has been observed in patients with unilateral Parkinsonism, suggesting that these sebum changes were likely regulated neuro-endocrinologically rather than purely neurologically [5,26,91]. Consistent with this notion, α-melanocyte stimulating hormone (α-MSH) levels were elevated in Parkinson patients, possibly due to inadequate dopaminergic input. Moreover, treatment with L-dopa reduced α-MSH, and re-established the synthesis of MSH-inhibiting factor, reducing sebum secretion [26,92].

Additionally, there is evidence for a link between neurological damage (e.g. traumatic brain, spinal cord injury) and SD [93]. Facial immobility of Parkinsonian patients (mask-like face) and immobility due to facial paralysis can induce elevated sebum accumulation and lead to SD, but only on the affected side [26,43,94]. Because poor hygiene has been implicated in SD, these observations suggest that sustained reservoirs of residual sebum associated with immobility may influence the manifestation of the disease [3,22,26,88]. SD is also more commonly seen in depressive disorders and emotional stress [5,16].

Other factors

In the past, nutrition has been studied as a possible contributing factor for SD. Zinc deficiency in patients with acrodermatitis enteropatica, riboflavin, pyridoxine and niacin deficiency can manifest seborrheicdermatitis-like rash [26,36]. Other medical conditions, such as familial amyloidotic polyneuropathy and Down syndrome, have also been associated with SD [95,96].

In summary, multiple predisposing factors have been identified in the pathogenesis of SD and dandruff (). The presence and abundance of Malassezia yeast, host epidermal conditions and sebaceous secretion, combined with various other factors, and interactions between these factors, determine an individual’s susceptibility to SD and dandruff. In a likely scenario, there may be aberrant epidermal barrier function due to genetic predisposition, and excessive or altered sebum composition would exacerbate EPB disruption and provides a favorable milieu for Malassezia colonization. Disrupted EPB function facilitates entry of Malassezia and its metabolites, and irritates the epidermis and elicits host’s immune response. The host inflammatory response further disturbs epidermal differentiation and barrier formation, and pruritus and subsequent scratching would damage the barrier even further, leading to cycles of immune stimulation, abnormal epidermal differentiation, and barrier disruption.

Predisposing factors and their interactions in the pathogenesis of seborrheic dermatitis and dandruff.

Conclusions

SD and dandruff are of a continuous spectrum of the same disease that affects the seborrheic areas of the body (). They share many common features and respond to similar treatments. Various intrinsic and environmental factors, such as Malassezia yeast, host epidermal conditions, sebaceous secretion, immune response, and the interactions between these factors, may all contribute to the pathogenesis. Effective management of SD and dandruff requires clearing of symptoms with antifungal and anti-inflammatory treatment, ameliorating associated symptoms such as pruritus, and general scalp and skin health to help maintain remission. Studies in humans and animal models to investigate the genetic and biochemical pathways will help identify new targets for the development of more efficacious treatment with less side effects, and better management of these conditions.

Table 4

Comparison of seborrheic dermatitis and dandruff.

Seborrheic Dermatitis Dandruff References
Epidemiology Up to 40% of infants within 3 months of age, 1–3% of the general adult population. 50% of adult population. [1–3,22,23]
Location Scalp, retro-auricular area, face (nasolabial folds, upper lip, eyelids, eyebrows), upper chest. Scalp. [2,7,15]
Presentation Erythematous patches, with large, oily or dry scales. White to yellow flakes dispersed on the scalp and hair; without erythema. [2,3,26]
Histology Acanthosis, hyperkeratosis, spongiosis, parakeratosis, Malassezia yeasts. [3,23,38]
Vasodilation and perivascular and perifollicular inflammatory infiltration; “shoulder parakeratosis”. Subtle neutrophil infiltration or no inflammatory infiltration.
Treatment Antifungal shampoos and topical. [2,8,26,47,97]
Topical corticosteroids, immune modulators, phototherapy, systemic treatment.
Predisposing Factors and causes Sebaceous gland activity, fungal colonization, and individual susceptibility (epidermal barrier integrity, host immune response, genetic factors, neurogenic factors and stress, nutrition, etc.). [2,3,9,15,26,44,66]

Abbreviations

AIDS Acquired Immune-Deficiency Syndrome
FTA-ABS Fluorescent Treponemal Antibody-Absorption
HAART Highly Active Antiretroviral Therapy
HIV Human Immune-Deficiency Virus
ICD Irritant Contact Dermatitis
QOL Quality of Life
RPR Rapid Plasma Regain
SC Stratum Corneum
SD Seborrheic Dermatitis
VDRL Venereal Disease Research Laboratory

Footnotes

Reviewed & Approved by: Dr. Craig G Burkhart, Clinical Professor, Department of Medicine, Ohio University, USA

References

1. Gupta AK, Madzia SE, Batra R. Etiology and management of Seborrheic dermatitis. Dermatology. 2004;208:89–93. [PubMed] [Google Scholar]2. Del Rosso JQ. Adult seborrheic dermatitis: a status report on practical topical management. J Clin Aesthet Dermatol. 2011;4:32–38. [PMC free article] [PubMed] [Google Scholar]3. Sampaio AL, Mameri AC, Vargas TJ, Ramos-e-Silva M, Nunes AP, et al. Seborrheic dermatitis. An Bras Dermatol. 2011;86:1061–1071. [PubMed] [Google Scholar]4. Schwartz RA, Janusz CA, Janniger CK. Seborrheic dermatitis: an overview. Am Fam Physician. 2006;74:125–130. [PubMed] [Google Scholar]5. Dessinioti C, Katsambas A. Seborrheic dermatitis: etiology, risk factors, and treatments: facts and controversies. Clin Dermatol. 2013;31:343–351. [PubMed] [Google Scholar]6. Foley P, Zuo Y, Plunkett A, Merlin K, Marks R. The frequency of common skin conditions in preschool-aged children in Australia: seborrheic dermatitis and pityriasis capitis (cradle cap) Arch Dermatol. 2003;139:318–322. [PubMed] [Google Scholar]7. Clark GW, Pope SM, Jaboori KA. Diagnosis and treatment of seborrheic dermatitis. Am Fam Physician. 2015;91:185–190. [PubMed] [Google Scholar]8. Naldi L, Rebora A. Clinical practice. Seborrheic dermatitis. N Engl J Med. 2009;360:387–396. [PubMed] [Google Scholar]9. Gupta AK, Bluhm R, Cooper EA, Summerbell RC, Batra R. Seborrheic dermatitis. Dermatol Clin. 2003;21:401–412. [PubMed] [Google Scholar]10. Dunic I, Vesic S, Jevtovic DJ. Oral candidiasis and seborrheic dermatitis in HIV-infected patients on highly active antiretroviral therapy. HIV Med. 2004;5:50–54. [PubMed] [Google Scholar]11. Lally A, Casabonne D, Newton R, Wojnarowska F. Seborrheic dermatitis among Oxford renal transplant recipients. J Eur Acad Dermatol Venereol. 2010;24:561–564. [PubMed] [Google Scholar]12. Ozcan D, Seckin D, Ada S, Haberal M. Mucocutaneous disorders in renal transplant recipients receiving sirolimus-based immunosuppressive therapy: a prospective, case-control study. Clin Transplant. 2013;27:742–748. [PubMed] [Google Scholar]13. Okada K, Endo Y, Fujisawa A, Tanioka M, Kabashima K, et al. Refractory seborrheic dermatitis of the head in a patient with malignant lymphoma. Case Rep Dermatol. 2014;6:279–282. [PMC free article] [PubMed] [Google Scholar]14. Nnoruka EN, Chukwuka JC, Anisuiba B. Correlation of mucocutaneous manifestations of HIV/AIDS infection with CD4 counts and disease progression. Int J Dermatol. 2007;46(Suppl 2):14–18. [PubMed] [Google Scholar]15. Ramos-E-Silva M, Sampaio AL, Carneiro S. Red face revisited: Endogenous dermatitis in the form of atopic dermatitis and seborrheic dermatitis. Clin Dermatol. 2014;32:109–115. [PubMed] [Google Scholar]16. Maietta G, Fornaro P, Rongioletti F, Rebora A. Patients with mood depression have a high prevalence of seborrhoeic dermatitis. Acta Derm Venereol. 1990;70:432–434. [PubMed] [Google Scholar]17. Mastrolonardo M, Diaferio A, Logroscino G. Seborrheic dermatitis, increased sebum excretion, and Parkinson’s disease: a survey of (im) possible links. Med Hypotheses. 2003;60:907–911. [PubMed] [Google Scholar]18. Barba A, Piubello W, Vantini I, Caliari S, Cocchetto R, et al. Skin lesions in chronic alcoholic pancreatitis. Dermatologica. 1982;164:322–326. [PubMed] [Google Scholar]19. Cribier B, Samain F, Vetter D, Heid E, Grosshans E. Systematic cutaneous examination in hepatitis C virus infected patients. Acta Derm Venereol. 1998;78:355–357. [PubMed] [Google Scholar]20. Bilgili SG, Akdeniz N, Karadag AS, Akbayram S, Calka O, et al. Mucocutaneous disorders in children with down syndrome: case-controlled study. Genet Couns. 2011;22:385–392. [PubMed] [Google Scholar]21. Tegner E. Seborrhoeic dermatitis of the face induced by PUVA treatment. Acta Derm Venereol. 1983;63:335–339. [PubMed] [Google Scholar]23. Schwartz JR, Cardin CW, Dawson TL. Seborrheic dermatitis and dandruff. In: Baran R, Maibach HI, editors. Textbook of Cosmetic dermatology. London: Martin Dunitz, Ltd; 2010. pp. 230–241. [Google Scholar]24. Bickers DR, Lim HW, Margolis D, Weinstock MA, Goodman C, et al. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology. J Am Acad Dermatol. 2006;55:490–500. [PubMed] [Google Scholar]25. Berg M. Epidemiological studies of the influence of sunlight on the skin. Photodermatol. 1989;6:80–84. [PubMed] [Google Scholar]26. Bukvic Mokos Z, Kralj M, Basta-Juzbasic A, Lakos Jukic I. Seborrheic dermatitis: an update. Acta Dermatovenerol Croat. 2012;20:98–104. [PubMed] [Google Scholar]27. Misery L, Touboul S, Vincot C, Dutray S, Rolland-Jacob G, et al. Stress and seborrheic dermatitis. Ann Dermatol Venereol. 2007;134:833–837. [PubMed] [Google Scholar]28. Szepietowski JC, Reich A, Wesolowska-Szepietowska E, Baran E, National Quality of Life in Dermatology Group Quality of life in patients suffering from seborrheic dermatitis: influence of age, gender and education level. Mycoses. 2009;52:357–363. [PubMed] [Google Scholar]29. Peyri J, Lleonart M, Grupo español del Estudio SEBDERM Clinical and therapeutic profile and quality of life of patients with seborrheic dermatitis. Actas Dermosifiliogr. 2007;98:476–482. [PubMed] [Google Scholar]30. Mathes BM, Douglass MC. Seborrheic dermatitis in patients with acquired immunodeficiency syndrome. J Am Acad Dermatol. 1985;13:947–951. [PubMed] [Google Scholar]31. Osei-Sekyere B, Karstaedt AS. Immune reconstitution inflammatory syndrome involving the skin. Clin Exp Dermatol. 2010;35:477–481. [PubMed] [Google Scholar]32. Boehncke WH. Etiology and pathogenesis of psoriasis. Rheum Dis Clin North Am. 2015;41:665–675. [PubMed] [Google Scholar]33. Meadows-Oliver M. Tinea capitis: diagnostic criteria and treatment options. Pediatr Nurs. 2009;35:53–57. [PubMed] [Google Scholar]34. Tuzun Y, Wolf R, Kutlubay Z, Karakus O, Engin B. Rosacea and rhinophyma. Clin Dermatol. 2014;32:35–46. [PubMed] [Google Scholar]35. Lisnevskaia L, Murphy G, Isenberg D. Systemic lupus erythematosus. Lancet. 2014;384:1878–1888. [PubMed] [Google Scholar]36. Valia RG. Etiopathogenesis of seborrheic dermatitis. Indian J Dermatol Venereol Leprol. 2006;72:253–255. [PubMed] [Google Scholar]37. Yamamoto T, Tsuboi R. Interleukin-2-induced seborrhoeic dermatitis-like eruption. J Eur Acad Dermatol Venereol. 2008;22:244–245. [PubMed] [Google Scholar]38. Reider N, Fritsch PO. Other eczematous eruptions. In: Bolognia JL, Jorizzo JL, Schaffer JV, editors. Dermatology. UK: Elsevier Health Sciences; 2012. pp. 219–221. [Google Scholar]39. Schwartz JR, Messenger AG, Tosti A, Todd G, Hordinsky M, et al. A comprehensive pathophysiology of dandruff and seborrheic dermatitis – towards a more precise definition of scalp health. Acta Derm Venereol. 2013;93:131–137. [PubMed] [Google Scholar]40. Pazyar N, Yaghoobi R, Bagherani N, Kazerouni A. A review of applications of tea tree oil in dermatology. Int J Dermatol. 2013;52:784–790. [PubMed] [Google Scholar]41. Satchell AC, Saurajen A, Bell C, Barnetson RS. Treatment of dandruff with 5% tea tree oil shampoo. J Am Acad Dermatol. 2002;47:852–855. [PubMed] [Google Scholar]42. Gaitanis G, Magiatis P, Hantschke M, Bassukas ID, Velegraki A. The Malassezia genus in skin and systemic diseases. Clin Microbiol Rev. 2012;25:106–141. [PMC free article] [PubMed] [Google Scholar]43. Hay RJ. Malassezia dandruff and seborrhoeic dermatitis: an overview. Br J Dermatol. 2011;165(Suppl 2):2–8. [PubMed] [Google Scholar]44. Ro BI, Dawson TL. The role of sebaceous gland activity and scalp microfloral metabolism in the etiology of seborrheic dermatitis and dandruff. J Investig Dermatol Symp Proc. 2005;10:194–197. [PubMed] [Google Scholar]45. Rudramurthy SM, Honnavar P, Dogra S, Yegneswaran PP, Handa S, et al. Association of Malassezia species with dandruff. Indian J Med Res. 2014;139:431–437. [PMC free article] [PubMed] [Google Scholar]46. Shuster S. The aetiology of dandruff and the mode of action of therapeutic agents. Br J Dermatol. 1984;111:235–242. [PubMed] [Google Scholar]48. DeAngelis YM, Gemmer CM, Kaczvinsky JR, Kenneally DC, Schwartz JR, et al. Three etiologic facets of dandruff and seborrheic dermatitis: Malassezia fungi, sebaceous lipids, and individual sensitivity. J Investig Dermatol Symp Proc. 2005;10:295–297. [PubMed] [Google Scholar]49. Heng MC, Henderson CL, Barker DC, Haberfelde G. Correlation of Pityosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique. J Am Acad Dermatol. 1990;23:82–86. [PubMed] [Google Scholar]50. McGinley KJ, Leyden JJ, Marples RR, Kligman AM. Quantitative microbiology of the scalp in non-dandruff, dandruff, and seborrheic dermatitis. J Invest Dermatol. 1975;64:401–405. [PubMed] [Google Scholar]51. DeAngelis YM, Saunders CW, Johnstone KR, Reeder NL, Coleman CG, et al. Isolation and expression of a Malassezia globosa lipase gene, LIP1. J Invest Dermatol. 2007;127:2138–2146. [PubMed] [Google Scholar]52. Plotkin LI, Squiquera L, Mathov I, Galimberti R, Leoni J. Characterization of the lipase activity of Malassezia furfur. J Med Vet Mycol. 1996;34:43–48. [PubMed] [Google Scholar]53. Warner RR, Schwartz JR, Boissy Y, Dawson TL., Jr Dandruff has an altered stratum corneum ultrastructure that is improved with zinc pyrithione shampoo. J Am Acad Dermatol. 2001;45:897–903. [PubMed] [Google Scholar]54. Faergemann J, Bergbrant IM, Dohse M, Scott A, Westgate G. Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry. Br J Dermatol. 2001;144:549–556. [PubMed] [Google Scholar]55. Breen PT. Canine seborrheic dermatitis. Vet Med Small Anim Clin. 1971;66:655–656. [PubMed] [Google Scholar]56. Eguchi-Coe Y, Valentine BA, Gorman E, Villarroel A. Putative Malassezia dermatitis in six goats. Vet Dermatol. 2011;22:497–501. [PubMed] [Google Scholar]57. Newcomer CE, Fox JG, Taylor RM, Smith DE. Seborrheic dermatitis in a rhesus monkey (Macaca mulatta) Lab Anim Sci. 1984;34:185–187. [PubMed] [Google Scholar]58. Pin D. Seborrhoeic dermatitis in a goat due to Malassezia pachydermatis. Vet Dermatol. 2004;15:53–56. [PubMed] [Google Scholar]59. Uzal FA, Paulson D, Eigenheer AL, Walker RL. Malassezia slooffiae-associated dermatitis in a goat. Vet Dermatol. 2007;18:348–352. [PubMed] [Google Scholar]60. Zouboulis CC, Akamatsu H, Stephanek K, Orfanos CE. Androgens affect the activity of human sebocytes in culture in a manner dependent on the localization of the sebaceous glands and their effect is antagonized by spironolactone. Skin Pharmacol. 1994;7:33–40. [PubMed] [Google Scholar]62. Strauss JS, Downing DT, Ebling FJ. Sebaceous glands. In: Goldsmith LA, editor. Biochemistry and physiology of skin. New York: Oxford University Press; 1983. pp. 569–595. [Google Scholar]64. Ostlere LS, Taylor CR, Harris DW, Rustin MH, Wright S, et al. Skin surface lipids in HIV-positive patients with and without seborrheic dermatitis. Int J Dermatol. 1996;35:276–279. [PubMed] [Google Scholar]65. Harding CR. The stratum corneum: structure and function in health and disease. Dermatol Ther. 2004;17(Suppl 1):6–15. [PubMed] [Google Scholar]67. Sheu HM, Chao SC, Wong TW, Yu-Yun Lee J, Tsai JC. Human skin surface lipid film: an ultrastructural study and interaction with corneocytes and intercellular lipid lamellae of the stratum corneum. Br J Dermatol. 1999;140:385–391. [PubMed] [Google Scholar]68. Simon M, Tazi-Ahnini R, Jonca N, Caubet C, Cork MJ, et al. Alterations in the desquamation-related proteolytic cleavage of corneodesmosin and other corneodesmosomal proteins in psoriatic lesional epidermis. Br J Dermatol. 2008;159:77–85. [PubMed] [Google Scholar]69. Harding CR, Moore AE, Rogers JS, Meldrum H, Scott AE, et al. Dandruff: a condition characterized by decreased levels of intercellular lipids in scalp stratum corneum and impaired barrier function. Arch Dermatol Res. 2002;294:221–230. [PubMed] [Google Scholar]70. Rukwied R, Zeck S, Schmelz M, McGlone F. Sensitivity of human scalp skin to pruritic stimuli investigated by intradermal microdialysis in vivo. J Am Acad Dermatol. 2002;47:245–250. [PubMed] [Google Scholar]71. Birnbaum RY, Zvulunov A, Hallel-Halevy D, Cagnano E, Finer G, et al. Seborrhea-like dermatitis with psoriasiform elements caused by a mutation in ZNF750, encoding a putative C2h3 zinc finger protein. Nat Genet. 2006;38:749–751. [PubMed] [Google Scholar]72. Kerr K, Darcy T, Henry J, Mizoguchi H, Schwartz JR, et al. Epidermal changes associated with symptomatic resolution of dandruff: biomarkers of scalp health. Int J Dermatol. 2011;50:102–113. [PubMed] [Google Scholar]73. Sampaio AL, Nunes AP. School of Medicine. Rio de Janeiro, Brazil: Federal University of Rio de Janeiro; 2011. Study of frequency of human leukocyte antigen (HLA) in seborrheic dermatitis patients in a miscegenated population. [Google Scholar]74. Tsuji K, Nose Y, Ito M, Ozala A, Matsuo I. HLA antigens and susceptibility to psoriasis vulgaris in a non-Caucasian population. Tissue Antigens. 1976;8:29–33. [PubMed] [Google Scholar]75. Bergbrant IM, Johansson S, Robbins D, Scheynius A, Faergemann J, et al. An immunological study in patients with seborrhoeic dermatitis. Clin Exp Dermatol. 1991;16:331–338. [PubMed] [Google Scholar]76. Parry ME, Sharpe GR. Seborrhoeic dermatitis is not caused by an altered immune response to Malassezia yeast. Br J Dermatol. 1998;139:254–263. [PubMed] [Google Scholar]77. Ashbee HR, Ingham E, Holland KT, Cunliffe WJ. Cell-mediated immune responses to Malassezia furfur serovars A, B and C in patients with pityriasis versicolor, seborrheic dermatitis and controls. Exp Dermatol. 1994;3:106–112. [PubMed] [Google Scholar]78. Bergbrant IM, Andersson B, Faergemann J. Cell-mediated immunity to Malassezia furfur in patients with seborrhoeic dermatitis and pityriasis versicolor. Clin Exp Dermatol. 1999;24:402–406. [PubMed] [Google Scholar]79. Neuber K, Kroger S, Gruseck E, Abeck D, Ring J. Effects of Pityrosporum ovale on proliferation, immunoglobulin (IgA, G, M) synthesis and cytokine (IL-2, IL-10, IFN gamma) production of peripheral blood mononuclear cells from patients with seborrhoeic dermatitis. Arch Dermatol Res. 1996;288:532–536. [PubMed] [Google Scholar]80. Hoger H, Gialamas J, Adamiker D. Inherited seborrheic dermatitis–a new mutant in mice. Lab Anim. 1987;21:299–305. [PubMed] [Google Scholar]81. Hoger H, Gialamas J, Adamiker D. Reduced tumour incidence in mice with inherited seborrhoeic dermatitis. Lab Anim. 1994;28:340–346. [PubMed] [Google Scholar]82. Oble DA, Collett E, Hsieh M, Ambjorn M, Law J, et al. A novel T cell receptor transgenic animal model of seborrheic dermatitis-like skin disease. J Invest Dermatol. 2005;124:151–159. [PubMed] [Google Scholar]83. Hayashi K, Cao T, Passmore H, Jourdan-Le Saux C, Fogelgren B, et al. Progressive hair loss and myocardial degeneration in rough coat mice: reduced lysyl oxidase-like (LOXL) in the skin and heart. J Invest Dermatol. 2004;123:864–871. [PubMed] [Google Scholar]84. Cao T, Racz P, Szauter KM, Groma G, Nakamatsu GY, et al. Mutation in Mpzl3, a novel [corrected] gene encoding a predicted [corrected] adhesion protein, in the rough coat (rc) mice with severe skin and hair abnormalities. J Invest Dermatol. 2007;127:1375–1386. [PMC free article] [PubMed] [Google Scholar]85. Leiva AG, Chen AL, Devarajan P, Chen Z, Damanpour S, et al. Loss of Mpzl3 function causes various skin abnormalities and greatly reduced adipose depots. J Invest Dermatol. 2014;134:1817–1827. [PMC free article] [PubMed] [Google Scholar]86. Bhaduri A, Ungewickell A, Boxer LD, Lopez-Pajares V, Zarnegar BJ, et al. Network analysis identifies mitochondrial regulation of epidermal differentiation by MPZL3 and FDXR. Dev Cell. 2015;35:444–457. [PMC free article] [PubMed] [Google Scholar]87. Burton JL, Cartlidge M, Cartlidge NE, Shuster S. Sebum excretion in parkinsonism. Br J Dermatol. 1973;88:263–266. [PubMed] [Google Scholar]88. Cowley NC, Farr PM, Shuster S. The permissive effect of sebum in seborrhoeic dermatitis: an explanation of the rash in neurological disorders. Br J Dermatol. 1990;122:71–76. [PubMed] [Google Scholar]89. Binder RL, Jonelis FJ. Seborrheic dermatitis in neuroleptic-induced parkinsonism. Arch Dermatol. 1983;119:473–475. [PubMed] [Google Scholar]90. Binder RL, Jonelis FJ. Seborrheic dermatitis: a newly reported side effect of neuroleptics. J Clin Psychiatry. 1984;45:125–126. [PubMed] [Google Scholar]91. Burton JL, Shuster S. Effect of L-dopa on seborrhoea of parkinsonism. Lancet. 1970;2:19–20. [PubMed] [Google Scholar]92. Burton JL, Cartlidge M, Shuster S. Effect of L-dopa on the seborrhoea of Parkinsonism. Br J Dermatol. 1973;88:475–479. [PubMed] [Google Scholar]93. Wilson CL, Walshe M. Incidence of seborrheic dermatitis in spinal injury patients. Br J Dermatol (suppl 33) 1988;119:48. [Google Scholar]94. Bettley FR, Marten RH. Unilateral seborrheic dermatitis following a nerve lesion. AMA Arch Derm. 1956;73:110–115. [PubMed] [Google Scholar]95. Ercis M, Balci S, Atakan N. Dermatological manifestations of 71 Down syndrome children admitted to a clinical genetics unit. Clin Genet. 1996;50:317–320. [PubMed] [Google Scholar]96. Rocha N, Velho G, Horta M, Martins A, Massa A. Cutaneous manifestations of familial amyloidotic polyneuropathy. J Eur Acad Dermatol Venereol. 2005;19:605–607. [PubMed] [Google Scholar]97. Hald M, Arendrup MC, Svejgaard EL, Lindskov R, Foged EK, et al. Evidence-based Danish guidelines for the treatment of Malassezia-related skin diseases. Acta Derm Venereol. 2015;95:12–19. [PubMed] [Google Scholar]98. Koc E, Arca E, Kose O, Akar A. An open, randomized, prospective, comparative study of topical pimecrolimus 1% cream and topical ketoconazole 2% cream in the treatment of seborrheic dermatitis. J Dermatolog Treat. 2009;20:4–9. [PubMed] [Google Scholar]99. Okokon EO, Verbeek JH, Ruotsalainen JH, Ojo OA, Bakhoya VN. Topical antifungals for seborrhoeic dermatitis. Cochrane Database Syst Rev. 2015;5:CD008138. [PMC free article] [PubMed] [Google Scholar]100. Peter RU, Richarz-Barthauer U. Successful treatment and prophylaxis of scalp seborrhoeic dermatitis and dandruff with 2% ketoconazole shampoo: results of a multicentre, double-blind, placebo-controlled trial. Br J Dermatol. 1995;132:441–445. [PubMed] [Google Scholar]101. Pierard-Franchimont C, Goffin V, Decroix J, Pierard GE. A multicenter randomized trial of ketoconazole 2% and zinc pyrithione 1% shampoos in severe dandruff and seborrheic dermatitis. Skin Pharmacol Appl Skin Physiol. 2002;15:434–441. [PubMed] [Google Scholar]102. Segal R, David M, Ingber A, Lurie R, Sandbank M. Treatment with bifonazole shampoo for seborrhea and seborrheic dermatitis: a randomized, double-blind study. Acta Derm Venereol. 1992;72:454–455. [PubMed] [Google Scholar]103. Faergemann J. Seborrhoeic dermatitis and Pityrosporum orbiculare: treatment of seborrhoeic dermatitis of the scalp with miconazole-hydrocortisone (Daktacort), miconazole and hydrocortisone. Br J Dermatol. 1986;114:695–700. [PubMed] [Google Scholar]104. Dupuy P, Maurette C, Amoric JC, Chosidow O, Study Investigator Group Randomized, placebo-controlled, double-blind study on clinical efficacy of ciclopiroxolamine 1% cream in facial seborrhoeic dermatitis. Br J Dermatol. 2001;144:1033–1037. [PubMed] [Google Scholar]105. Ratnavel RC, Squire RA, Boorman GC. Clinical efficacies of shampoos containing ciclopirox olamine (1.5%) and ketoconazole (2.0%) in the treatment of seborrhoeic dermatitis. J Dermatolog Treat. 2007;18:88–96. [PubMed] [Google Scholar]106. Danby FW, Maddin WS, Margesson LJ, Rosenthal D. A randomized, double-blind, placebo-controlled trial of ketoconazole 2% shampoo versus selenium sulfide 2.5% shampoo in the treatment of moderate to severe dandruff. J Am Acad Dermatol. 1993;29:1008–1012. [PubMed] [Google Scholar]107. Gilbertson K, Jarrett R, Bayliss SJ, Berk DR. Scalp discoloration from selenium sulfide shampoo: a case series and review of the literature. Pediatr Dermatol. 2012;29:84–88. [PubMed] [Google Scholar]108. Reeder NL, Xu J, Youngquist RS, Schwartz JR, Rust RC, et al. The antifungal mechanism of action of zinc pyrithione. Br J Dermatol. 2011;165(Suppl 2):9–12. [PubMed] [Google Scholar]109. Shin H, Kwon OS, Won CH, Kim BJ, Lee YW, et al. Clinical efficacies of topical agents for the treatment of seborrheic dermatitis of the scalp: a comparative study. J Dermatol. 2009;36:131–137. [PubMed] [Google Scholar]110. Ortonne JP, Lacour JP, Vitetta A, Le Fichoux Y. Comparative study of ketoconazole 2% foaming gel and betamethasone dipropionate 0.05% lotion in the treatment of seborrhoeic dermatitis in adults. Dermatology. 1992;184:275–280. [PubMed] [Google Scholar]111. Elewski B. An investigator-blind, randomized, 4-week, parallel-group, multicenter pilot study to compare the safety and efficacy of a nonsteroidal cream (Promiseb Topical Cream) and desonide cream 0.05% in the twice-daily treatment of mild to moderate seborrheic dermatitis of the face. Clin Dermatol. 2009;27(6 Suppl):S48–S53. [PubMed] [Google Scholar]112. Kircik LH. Treatment of scalp and facial seborrheic dermatitis with desonide hydrogel 0.05% J Clin Aesthet Dermatol. 2009;2:32–36. [PMC free article] [PubMed] [Google Scholar]113. Pierard-Franchimont C, Pierard GE. A double-blind placebo-controlled study of ketoconazole + desonide gel combination in the treatment of facial seborrheic dermatitis. Dermatology. 2002;204:344–347. [PubMed] [Google Scholar]114. Kircik L. The evolving role of therapeutic shampoos for targeting symptoms of inflammatory scalp disorders. J Drugs Dermatol. 2010;9:41–48. [PubMed] [Google Scholar]115. Cook BA, Warshaw EM. Role of topical calcineurin inhibitors in the treatment of seborrheic dermatitis: a review of pathophysiology, safety, and efficacy. Am J Clin Dermatol. 2009;10:103–118. [PubMed] [Google Scholar]116. Kim BS, Kim SH, Kim MB, Oh CK, Jang HS, et al. Treatment of facial seborrheic dermatitis with pimecrolimus cream 1%: an open-label clinical study in Korean patients. J Korean Med Sci. 2007;22:868–872. [PMC free article] [PubMed] [Google Scholar]117. Ozden MG, Tekin NS, Ilter N, Ankarali H. Topical pimecrolimus 1% cream for resistant seborrheic dermatitis of the face: an open-label study. Am J Clin Dermatol. 2010;11:51–54. [PubMed] [Google Scholar]118. Thaci D, Salgo R. Malignancy concerns of topical calcineurin inhibitors for atopic dermatitis: facts and controversies. Clin Dermatol. 2010;28:52–56. [PubMed] [Google Scholar]119. Kim HO, Yang YS, Ko HC, Kim GM, Cho SH, et al. Maintenance therapy of facial seborrheic dermatitis with 0.1% tacrolimus ointment. Ann Dermatol. 2015;27:523–530. [PMC free article] [PubMed] [Google Scholar]120. Papp KA, Papp A, Dahmer B, Clark CS. Single-blind, randomized controlled trial evaluating the treatment of facial seborrheic dermatitis with hydrocortisone 1% ointment compared with tacrolimus 0.1% ointment in adults. J Am Acad Dermatol. 2012;67:e11–e15. [PubMed] [Google Scholar]121. Davies DB, Boorman GC, Shuttleworth D. Comparative efficacy of shampoos containing coal tar (4.0% w/w; Tarmed™), coal tar (4.0% w/w) plus ciclopirox olamine (1.0% w/w; Tarmed™ AF) and ketoconazole (2.0% w/w; Nizoral™) for the treatment of dandruff/seborrhoeic dermatitis. J Dermatolog Treat. 1999;10:177–183. [Google Scholar]122. Ballanger F, Tenaud I, Volteau C, Khammari A, Dreno B. Anti-inflammatory effects of lithium gluconate on keratinocytes: a possible explanation for efficiency in seborrhoeic dermatitis. Arch Dermatol Res. 2008;300:215–223. [PubMed] [Google Scholar]123. Dreno B, Moyse D. Lithium gluconate in the treatment of seborrhoeic dermatitis: a multicenter, randomised, double-blind study versus placebo. Eur J Dermatol. 2002;12:549–552. [PubMed] [Google Scholar]124. Stefanaki I, Katsambas A. Therapeutic update on seborrheic dermatitis. Skin Therapy Lett. 2010;15:1–4. [PubMed] [Google Scholar]125. Koca R, Altinyazar HC, Esturk E. Is topical metronidazole effective in seborrheic dermatitis? A double-blind study. Int J Dermatol. 2003;42:632–635. [PubMed] [Google Scholar]126. Seckin D, Gurbuz O, Akin O. Metronidazole 0.75% gel vs. ketoconazole 2% cream in the treatment of facial seborrheic dermatitis: a randomized, double-blind study. J Eur Acad Dermatol Venereol. 2007;21:345–350. [PubMed] [Google Scholar]127. Lee E, Koo J, Berger T. UVB phototherapy and skin cancer risk: a review of the literature. Int J Dermatol. 2005;44:355–360. [PubMed] [Google Scholar]128. Pirkhammer D, Seeber A, Honigsmann H, Tanew A. Narrow-band ultraviolet B (ATL-01) phototherapy is an effective and safe treatment option for patients with severe seborrhoeic dermatitis. Br J Dermatol. 2000;143:964–968. [PubMed] [Google Scholar]130. Das J, Majumdar M, Chakraborty U, Majumdar V, Mazumdar G, et al. Oral itraconazole for the treatment of severe seborrhoeic dermatitis. Indian J Dermatol. 2011;56:515–516. [PMC free article] [PubMed] [Google Scholar]131. Kose O, Erbil H, Gur AR. Oral itraconazole for the treatment of seborrhoeic dermatitis: an open, noncomparative trial. J Eur Acad Dermatol Venereol. 2005;19:172–175. [PubMed] [Google Scholar]132. Gupta AK, Richardson M, Paquet M. Systematic review of oral treatments for seborrheic dermatitis. J Eur Acad Dermatol Venereol. 2014;28:16–26. [PubMed] [Google Scholar]133. Scaparro E, Quadri G, Virno G, Orifici C, Milani M. Evaluation of the efficacy and tolerability of oral terbinafine (Daskil) in patients with seborrhoeic dermatitis. A multicentre, randomized, investigator-blinded, placebo-controlled trial. Br J Dermatol. 2001;144:854–857. [PubMed] [Google Scholar]134. Vena GA, Micali G, Santoianni P, Cassano N, Peruzzi E. Oral terbinafine in the treatment of multi-site seborrhoic dermatitis: a multicenter, double-blind placebo-controlled study. Int J Immunopathol Pharmacol. 2005;18:745–753. [PubMed] [Google Scholar]

Seborrhoeic dermatitis | DermNet NZ

Author: A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand, 1997. Latest update by Dr Jannet Gomez, October 2017.


What is seborrhoeic dermatitis?

Seborrhoeic dermatitis (American spelling is ‘seborrheic’) is a common, chronic or relapsing form of eczema/dermatitis that mainly affects the sebaceous, gland-rich regions of the scalp, face, and trunk . 

There are infantile and adult forms of seborrhoeic dermatitis. It is sometimes associated with psoriasis (sebopsoriasis). Seborrhoeic dermatitis is also known as seborrhoeic eczema.

Dandruff (also called ‘pityriasis capitis’) is an uninflamed form of seborrhoeic dermatitis. Dandruff presents as bran-like scaly patches scattered within hair-bearing areas of the scalp.

What causes seborrhoeic dermatitis?

The cause of seborrhoeic dermatitis is not completely understood. It is associated with proliferation of various species of the skin commensal Malassezia, in its yeast (non-pathogenic) form. Its metabolites (such as the fatty acids oleic acid, malssezin, and indole-3-carbaldehyde) may cause an inflammatory reaction. Differences in skin barrier lipid content and function may account for individual presentations.

Who gets seborrhoeic dermatitis?

Infantile seborrhoeic dermatitis affects babies under the age of 3 months and usually resolves by 6–12 months of age.

Adult seborrhoeic dermatitis tends to begin in late adolescence. Prevalence is greatest in young adults and in older people. It is more common in males than in females.

The following factors are sometimes associated with severe adult seborrhoeic dermatitis:

  • Oily skin (seborrhoea)
  • Familial tendency to seborrhoeic dermatitis or a family history of psoriasis
  • Immunosuppression: organ transplant recipient, human immunodeficiency virus (HIV) infection and patients with lymphoma
  • Neurological and psychiatric diseases: Parkinson disease, tardive dyskinesia, depression, epilepsy, facial nerve palsy, spinal cord injury, and congenital disorders such as Down syndrome
  • Treatment for psoriasis with psoralen and ultraviolet A (PUVA) therapy 
  • Lack of sleep, and stressful events.

What are the clinical features of seborrhoeic dermatitis?

Infantile seborrhoeic dermatitis

Infantile seborrhoeic dermatitis causes cradle cap (diffuse, greasy scaling on scalp). The rash may spread to affect armpit and groin folds (a type of napkin dermatitis).

  • There are salmon-pink patches that may flake or peel.
  • It is not especially itchy, so the baby often appears undisturbed by the rash, even when generalised.

Infantile seborrhoeic dermatitis

Adult seborrhoeic dermatitis

Seborrhoeic dermatitis affects scalp, face (creases around the nose, behind ears, within eyebrows) and upper trunk.

Typical features include:

  • Winter flares, improving in summer following sun exposure
  • Minimal itch most of the time
  • Combination oily and dry mid-facial skin
  • Ill-defined localised scaly patches or diffuse scale in the scalp
  • Blepharitis: scaly red eyelid margins
  • Salmon-pink, thin, scaly, and ill-defined plaques in skin folds on both sides of the face
  • Petal or ring-shaped flaky patches on hair-line and on anterior chest
  • Rash in armpits, under the breasts, in the groin folds, and genital creases
  • Superficial folliculitis (inflamed hair follicles) on cheeks and upper trunk.

Extensive seborrhoeic dermatitis affecting scalp, neck and trunk is sometimes called pityriasiform seborrhoeide.

Seborrhoeic dermatitis

How is seborrhoeic dermatitis diagnosed?

Seborrhoeic dermatitis is diagnosed by its clinical appearance and behaviour. As malassezia are a normal component of skin flora, their presence on microscopy of skin scrapings is not diagnostic.

Skin biopsy may be helpful but is rarely indicated. Histological findings specific to seborrhoeic dermatitis are superficial perivascular and perifollicular inflammatory infiltrates, psoriasiform hyperplasia, and parakeratosis around follicular openings.

What is the treatment for seborrhoeic dermatitis?

Treatment of seborrhoeic dermatitis often involves several of the following options.

In resistant cases in adults, oral itraconazole, tetracycline antibiotics or phototherapy may be recommended. Low dose oral isotretinoin has also been shown to be effective for severe or moderate seborrhoeic dermatitis.

Scalp treatment

Face, ears, chest and back

  • Cleanse the affected skin thoroughly once or twice each day using a non-soap cleanser.
  • Apply ketoconazole or ciclopirox cream once daily for 2 to 4 weeks, repeated as necessary.
  • Hydrocortisone cream can also be used, applied up to twice daily for 1 or 2 weeks. Occasionally a more potent topical steroid may be prescribed.
  • Topical calcineurin inhibitors such as pimecrolimus cream or tacrolimus ointment may be used instead of topical steroids.
  • A variety of herbal remedies are commonly used, but their efficacy is uncertain.

Management in infants

Regular washing of the scalp with baby shampoo or aqueous cream is followed by gentle brushing to clear the scales.

  • White petrolatum may be useful.  
  • Topical antifungals are often prescribed, depending on the extent of the rash.

 

References

  • Borda LJ, Wikramanayake TC. Seborrheic dermatitis and dandruff: a comprehensive review. J Clin Investig Dermatol. 2015;3(2):10.13188/2373-1044.1000019. doi:10.13188/2373-1044.1000019. PubMed Central.
  • de Souza Leão Kamamoto C, Sanudo A, Hassun KM, Bagatin E. Low-dose oral isotretinoin for moderate to severe seborrhea and seborrheic dermatitis: a randomized comparative trial. Int J Dermatol. 2017;56(1):80-5. doi:10.1111/ijd.13408. PubMed.
  • Cheong WK, Yeung CK, Torsekar RG, et al. Treatment of seborrhoeic dermatitis in Asia: a consensus guide. Skin Appendage Disord. 2016;1(4):187-96. doi:10.1159/000444682. PubMed Central.
  • Shenefelt PD. Herbal Treatment for Dermatologic Disorders. In: Benzie IFF, Wachtel-Galor S, editors. Herbal Medicine: Biomolecular and Clinical Aspects. 2nd edition.
  • Boca Raton (FL): CRC Press/Taylor & Francis; 2011. Chapter 18. Available from: https://www.ncbi.nlm.nih.gov/books/NBK92761/
  • Barak-Shinar D, Del Río R, Green LJ. Treatment of seborrheic dermatitis using a novel herbal-based cream. J Clin Aesthet Dermatol. 2017;10(4):17-23. PubMed Central.

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90,000 causes of occurrence, methods of treatment in the MEDSI clinic

Contents

Dandruff is characterized by the appearance of a large number of loose scales on the scalp, while they predominate in the occipito-parietal region. In most cases, it is a companion of seborrhea, but an important factor is also a hereditary predisposition (features of the structure of the skin and its secretion). The occurrence of dandruff can be associated with a violation of metabolic processes in the body, including improper hair care.It is sometimes viewed as an infectious disease.

The cells of the scalp are renewed every 28 days, while the old cells remain on the surface of the skin as dead keratinized scales. As a rule, dandruff is invisible, but the use of low-quality shampoos, regular drying and blow-drying of hair, including stress and illness, can lead to too frequent renewal of scalp cells and, as a result, to the appearance of a large amount of dandruff.

This Problem worries both women and men.According to experts, every third person suffers from this disease. The causes of dandruff can be: improper hair care, dry scalp, lack of vitamins A and B, nervous strain, gastrointestinal tract disorders, psychoemotional stressful situations, diseases of the endocrine system, as well as fungal diseases.

Small flaky scales of dry dandruff are distributed over the entire surface of the scalp or are concentrated in the parietal and frontal regions.Sebum production decreases, itchy skin worries, hair over time becomes dry, brittle and begins to fall out vigorously.

When dandruff occurs due to increased sebum secretion, characteristic of seborrhea, the scales become saturated with the secretion of the sebaceous glands, begin to exfoliate and acquire a yellowish color, while the hair quickly becomes dirty and sticks together, becomes greasy, often accompanied by itching of the scalp. In this case, the fat clogs the ducts of the sebaceous and sweat glands and irritates the nerve endings; this is also facilitated by fatty acids formed as a result of the decomposition and oxidation of fats; which further leads to hair loss and thinning.

Dandruff is a rather alarming symptom of hair disease and disorder in the body itself, therefore, at the slightest sign of it, it is recommended to consult a specialist and immediately begin to fight this scourge.

Oily seborrhea

Most often, there are cases of oily (thick or liquid) seborrhea. Fatty – due to an increase in the secretion of the sebaceous glands, which is directly related to an increase in the level of androgens. As a result, the composition of sebum changes, and this in turn leads to a decrease in its sterilizing properties, as well as the creation of favorable conditions for the development of microorganisms and skin lesions.The manifestations of the disease are more pronounced in areas of the skin where the sebaceous glands are located in large numbers: face, scalp, chest, back. At the same time, the skin takes on a gray-yellow color, becomes shiny and coarse, its porosity increases.

With a thick form of the disease, the hair becomes coarse and coarse. Thick oily seborrhea is characterized by hardening and a decrease in skin elasticity, a significant expansion of the sebaceous gland orifices. With liquid oily – the skin resembles an orange peel, sebum is excreted in excess from the sebaceous glands.The hair on the head seems to be oiled, and often stick together in strands.

After shampooing, on the second or third day, the hair becomes untidy, becomes greasy and often sticks together into oily strands. Dandruff from oily scales forms on the scalp, which is easily scraped off with a fingernail. Hair loss gradually increases, ending in a relatively short time (3-5 years, sometimes more) with significant baldness. In this case, it is already impossible to restore the hairline.

When trying to get rid of the manifestations of this disease, patients wash their hair more often, but these measures do not give the desired effect – the hair quickly becomes greasy. In addition, frequent shampooing provokes an even greater function of the sebum, and as a result, the hair becomes dirty even faster. Oily seborrhea is accompanied by severe itching of the skin, oily dandruff scales stick together, forming gray-yellowish plaques on the hair, falling from the hair onto the shoulders and giving the clothes an untidy look.

The cause may also be a yeast that has settled in the sebaceous gland. Itchy skin and increased greasiness of the skin, dandruff can be the results of its vigorous activity.

Dry seborrhea

In the dry form, reduced sebum secretion is observed, the scales almost completely cover the scalp and hair.

With this disease, the hair gradually becomes thinner, loses its shine, becomes brittle, breaks off and splits at the ends, and begins to fall out vigorously.Dandruff appears on the scalp in the form of easily crumbling, dry, whitish scales. The disease is often accompanied by itching.

Attempts to get rid of such phenomena by more frequent shampooing do not give the desired result, and most often even worsen the condition. This is understandable since dry skin is the main symptom. Therefore, all products that degrease the skin and hair are only harmful.

Seborrheic dermatitis (eczema)

Such dermatitis most often affects those parts of the body in which the sebaceous glands are most developed – this is primarily the scalp, natural folds (nasolabial, nasal, axillary, cervical, inguinal and behind the ear), back and chest.

Seborrhea and associated neuroendocrine disorders predispose to the development of dermatitis (eczema). It is known that seborrheic dermatitis is greatly exacerbated by emotional stress. The disease is characterized by reddish spots and plaques formed from erythematous-scaly spots with confluent miliary papules of yellowish-brown color. These rashes contribute to the appearance of ring-shaped garland-like outlines, sometimes of a bizarre shape.

In severe form, the disease can lead to erythroderma, involving the skin of the trunk and extremities in the pathological process.During puberty, as well as in adult patients, the following are affected: scalp, forehead, interscapular skin, less often limbs, behind the ear folds. On the scalp, eczema is characterized by dryness, pityriasis peeling, foci of reddening of the skin, serous-purulent or serous-hemorrhagic crusts, when removed, a continuous weeping surface is exposed.

The defeat behind the ear folds most often contributes to the manifestation of erythema, edema, deep painful cracks in the depths of the folds, oozing and yellow scales (or scales-crusts).On the body and limbs, there are yellowish-pink scaly spots with clear boundaries and sometimes small-knotted elements in the center of the lesion. Often complicated by the addition of a secondary infection (ostiofolliculitis is a small hemispherical pustule that occurs in the hair follicle and is penetrated in the center by the hair, with a peripheral erythematous rim), and during puberty, as well as in patients from 18 to 25 years old, they are combined with acne.

Seborrheic keratosis

The disease of keratosis (or basal cell papillomas) is a type of seborrhea.This condition is also called seborrheic keratoma, seborrheic wart, or senile wart. This keratosis is a benign tumor that occurs on the surface of the epidermis and never degenerates into malignant tumors. In the overwhelming majority of cases, this disease affects men over the age of 30. The disease is represented by many flat nodules that are covered with hard brown scales.

This type of keratosis is caused by the appearance of yellowish spots on the surface of the skin, especially often affecting the trunk and formed mainly in middle-aged people; over time, these spots slowly darken and take on the appearance of warts.

Treatment of seborrhea

When treating, first of all, it is necessary to identify and eliminate the causes of the disease. In this case, you need to consult with a trichologist to find out the severity of the disease in your case.

Effective treatment of seborrhea and its varieties is possible only with an integrated approach. For example, in the treatment of dermatitis, well-known folk and homeopathic remedies do not help to fully cure the disease. In this case, you need to seek advice from professionals in this field.

Eczema panel (e1 – Cat, dandruff; e5 – Dog, dandruff; d1 – House dust mite Dermatophagoides pteronyssinus; f13 – Peanuts; f14 – Soybeans; f4 – Wheat; f3 – Atlantic cod; f24 – Northern shrimp; f1 – Egg white; f2 – Cow’s milk)

Method of determination
Immunofluorescence assay (ImmunoCAP).

Study material
Blood serum

A comprehensive study is designed to identify possible triggering allergens in case of suspected atopic dermatitis (atopic eczema, neurodermatitis).A separate answer for each allergen.

Atopic dermatitis / eczema is an allergic skin disease that usually occurs in early childhood in persons with a hereditary predisposition. Food allergens (proteins of cow’s milk, chicken eggs, fish, cereals) play an important role in its development in childhood. The prevalence among children and adolescents in developed countries is 10-37%, among adults 0.2-2%. With age, food sensitization can transform into sensitization to inhalation allergens (house dust allergens, including house dust mites, animal allergens, plant pollen, fungal allergens).In 10-20% of patients with a typical clinical picture, the non-allergic nature of the disease is established.

Patient history, clinical examination, clarification of the nature of the symptoms help the doctor to establish the presumptive diagnosis, as well as (if allergy is suspected) to highlight the likely individually significant allergens. However, it is often impossible to make a diagnosis only on the basis of clinical signs and patient history; additional objective data are needed to confirm the likelihood of an allergy or to exclude this diagnosis.

For this purpose, for children, the screening test Phadiatop ImmunoCAP or Phadiatop Infant ImmunoCAP (using balanced mixtures of the most significant allergens for adults or children, with a general response to the mixture – see description of tests No. 6802PH and No. 6801PI) can initially be used. If it is positive, confirming the likelihood of the allergic nature of the disease, then a panel of tests can be applied that identify specific IgE to individual allergens. The choice of allergens for this test panel is determined by data on the prevalence of sensitization to individual allergens and the significance of various allergens as triggers for allergic reactions.

Detection of IgE sensitization to certain allergens, in combination with the established fact of clinical manifestations in response to these allergens, allows the doctor to diagnose allergies.

90,000 Dandruff, seborrheic eczema and Aloe Vera

Aloe Vera in scalp health.

Every day, in the process of natural renewal, the scalp cells are exfoliated. This usually happens unnoticed by us.But the picture changes completely if a fungal infection occurs. Depending on its degree, it can give different symptoms – from the appearance of scales to seborrheic eczema. In this case, dandruff is no longer just a cosmetic problem.

Normally functioning sebaceous glands provide softness and elasticity to the stratum corneum, maintain a certain pH level, thus protecting healthy skin from bacterial and fungal infections.

However, if you change – in one direction or another – the amount and composition of the secretion produced by the sebaceous glands, this protective layer may be disturbed.And now the vulnerable scalp becomes an excellent breeding ground for bacteria and fungi. The main troublemakers are yeast (pityriasis). They are normally found in the natural flora of the skin. However, when things get out of hand, these fungi can cause itching and inflammation. As a measure of self-defense, the scalp begins to actively exfoliate the cells of the epidermis. Often this process is delayed, and the clumps of cells flake off in the form of dandruff.If the problem is not pronounced, then they talk about simple peeling of the scalp. If, in addition, it is accompanied by redness and itching, then these are the classic symptoms of seborrheic eczema, which can affect all areas of the skin rich in sebaceous glands. Oily seborrhea can appear on the face, neck, chest, and upper back.

The most common cause of seborrheic eczema is the advanced form of common seborrhea. In addition, the disease often develops due to disruption of the normal functioning of the endocrine system.And just a weakened immune system, especially in children, with a certain proportion of the body’s predisposition, can lead to seborrheic dermatitis.

In addition, a number of other diseases can cause seborrheic dermatitis. Doctors refer to such ailments:

  • The presence of chronic fatigue syndrome, or constant emotional stress;
  • Disruption of the normal functioning of the gastrointestinal tract;
  • Disruption of the liver and gallbladder;
  • Diseases of the vegetative-vascular system, in particular vegetative-vascular dystonia;
  • Disruption of the normal functioning of the endocrine system.

Usually, itching and fungal infections can be easily treated with appropriate medications.

If you cannot cope with this problem using traditional methods and means, then Aloe Vera can come to the rescue.

Aloe Vera for seborrheic eczema, dermatitis and pruritus

Natural remedies can be effective in treating neurodermatitis or pruritus or similar situations if you use both external and internal cleansers at the same time.The most common mistake is using only ointments. And it doesn’t matter if eczema on the hands or its other localization is worried. Drinking Aloe Vera Gel and washing and moisturizing products based on Aloe Vera (shampoo, soap, shower gel, lotion, creams) will cope with the task.

We recommend to apply externally Aloe Vera intensive body cream – an innovative cream for the care of hypersensitive and problem skin, Aloe Vera cream with Propolis, Aloe Vera gel concentrate, Aloe Vera Spray.Aloe Vera creams are useful for relieving acute inflammation, itching and enhancing epidermal regeneration. With prolonged use of the emulsion, the dryness of the skin is significantly reduced, its elasticity increases.

Remember that real help is possible only with a high concentration of Aloe Vera itself in a particular product. If you want to influence the functions of the immune system with drinking Aloe Vera gel, you must reckon with the treatment for at least three months, and most likely with an even longer period.Leading Czech immunologist Assoc. Bystron from the Faculty Hospital in Olomouc writes in his book “ABOUT IMMUNITY” that the effect of the drug after immunomodulation is manifested after three months. Therefore, there is no point in buying one bottle of drinking Aloe Vera gel for a sample, taking the medicine with teaspoons over the next few months and expecting a significant change in health. We would not recommend doing this.

Pay close attention to your diet – limit the use of citrus fruits, spicy and spicy dishes, mushrooms.A dairy-plant diet is recommended. The use of Aloe Vera drinking gel will have a beneficial effect on the body as a whole. With the help of Aloe Vera, you will maintain a normal diet, maintain the intestinal microflora (which is important in eczema), and maintain a normal tone of the nervous system. Aloe Vera helps cleanse the intestines and liver.

Is it possible not to take the Aloe Vera drinking gel, but to be limited to external agents? This is what most people treating in the old-fashioned way do, and therefore they walk with a diagnosis of eczema, neurodermatitis, itchy skin all their lives, sometimes with improvement, sometimes with deterioration.

The use of products based on Aloe Vera may not completely eliminate the problem, and dandruff and itching will appear, but less often and insignificant. If you stop using Aloe Vera, then after a couple of weeks the situation may worsen again, so feed your body constantly, it will only get better.

The problems of seborrheic eczema do not pose a threat to life, but still it is an unpleasant thing that can cause embarrassment and discomfort, therefore Aloe Vera for this case is an effective solution with a fairly stable effect.

For more information on the treatment of eczema, see the article: Neurodermatitis, Eczema, Itchy Skin and Aloe Vera.

Examples of recoveries

Story 1: seborrheic eczema. Sigurd, who has had itchy scalp for many years, was diagnosed with seborrheic eczema. He regularly used prescribed ointments and shampoos, sometimes supplementing them with steroid creams and other ointments. Treatment brought short-term benefits: itching and inflammation stopped only for a while.Over the years of illness, Sigurd tried many natural remedies and medicines, but they did not give a lasting result.

One day, on the advice of a friend, he decided to start drinking Aloe Vera gel and use Aloe Vera shampoo. Over the next two months, his condition gradually improved and his scalp became healthier than ever before. Sigurd believes that he owes the improvement of his condition entirely to Aloe Vera and that, thanks to this plant, if he now has dandruff and itching, it is rare and insignificant.And if you stop using Aloe Vera, then after a couple of weeks the situation gets worse.

Story 2: Skin problems. From 1987 to 1990, Sheila and her husband lived in Cyprus, and there their four-year-old son Jack had problems: the skin on both cheekbones, just below the eyes, became very dry and covered with scales. They tried different mild moisturizers, but it only got worse: now the area around the ears and scalp are covered with scales. When they arrived in their home country on vacation, Sheila took the boy to a doctor, who examined him and prescribed a steroid face cream and scalp fluid.From the cream, dry, scaly skin turned bright red, shiny, irritated, which only exacerbated the problem.

Sheila says: “We continued to apply the cream, hoping that over time it would have a positive effect. The prescribed liquid was so strong that it damaged the scalp, and we gave it up. The cream did not help at all, and we returned it to the doctor, who instead prescribed another remedy – a mild water-based cream, which also turned out to be useless.This was the first visit to the doctor and the first drugs in the long, long chain that followed. The situation dragged on for five years, and over the years, Jack’s skin condition has steadily deteriorated. We have tried all kinds of creams and a huge variety of products, but none of them has given the slightest positive effect. Our son was constantly teased at school because dry scales on the scalp looked like dandruff. To top it off, Jack, who had previously preferred short hedgehog cuts, wanted to grow his hair out to hide problem skin.Children at school nicknamed him “the scabby pig” – they say, he rarely washes his hair. You can imagine what it was like for your son to listen to the mockery! He was fed up with them.

In 1995, my brother’s wife told us about a new line of products based on Aloe Vera and advised us to try a face cream with Aloe Vera and bee propolis. It was very pleasant, finally, to deal with a natural remedy without any “chemistry”. It certainly could not be harmful, which cannot be said about some of the steroid drugs that were prescribed to Jack.We tried to apply the cream three times a day. The result stunned us. After about a week, no dry skin remains on the face. It was hard to believe that our problem was solved so quickly – and this after five years of senseless visits to doctors, using all conceivable and inconceivable creams. Shortly before that, we made an appointment with a dermatologist and decided to apply the cream with Aloe Vera and propolis so far only on the face, and not touch the scalp and show the doctor “in all its glory” so that he could establish the cause of the disease.Impressed by the effect of the Aloe Vera and Propolis cream, we took the tube to the doctor to show her the remedy that helped us heal our facial skin. After examining Jack’s scalp, the specialist (to my indignation, since I knew for sure that this was not the case) suggested that his son had lice. She took the scraping and asked to call her tomorrow. She really did not find lice (which we told her), and, unfortunately, the cause of the problem, too. And she prescribed us another shampoo, which we did not even think of buying: we had already gone through all this useless gimp.Instead, we chose to start using other products of the same brand recommended by my brother’s sister for scalp treatment, namely Aloe Vera shampoo and the same conditioner.

After a short time, we noticed an incredible improvement and decided to continue using these two products. Currently, the scalp is completely cleansed, and we forgot about the problems with it, just like a little earlier we forgot about the problems with the skin of the face. ”

Story 3: seborrheic dermatitis.”I want to tell you how with the help of Aloe Vera my sister” defeated “seborrheic dermatitis. The photo of people suffering from this disease, especially in its severe forms, is a little scary. But my sister’s seborrheic dermatitis was not so pronounced and manifested itself in the form of dandruff Locally, she applied a solution consisting of aloe juice with the addition of alcohol in a ratio (5: 1). The procedure was repeated every other day for two and a half months. I want to note that not only all signs of seborrhea disappeared from her, but the condition of the hair has also improved. “

Dandruff | Central Clinic

Many people are familiar with such a nuisance as dandruff. It is a common scalp disease and affects more than half of all people on earth, both men and women.

What is dandruff?

This is an increased exfoliation of the scaly layer of the skin, a mild form of seborrheic dermatitis. Appears with excessive sebum production of the skin of the scalp (seborrhea).It can also appear due to metabolic disorders, as a result of which seborrhea or fungus appears. Both can often be diagnosed.

The simplest signs of dandruff are white scales on the shoulders and hair, but there are other signs:

  • itching;
  • redness;
  • dry scalp.

What causes of dandruff can be identified

  1. Hormonal. The amount and composition of sebum depends on the state of the body as a whole, especially on the work of the endocrine and digestive systems.The hormonal background, or rather the balance between male and female hormones, also affects the secretion of sebaceous secretions. With an increase in male hormones (androgens), changes in sebum secretion occur. There is also a large fat content of the skin of the face, back, chest. This often occurs between the ages of 15-25. Also, with age, the amount of the hormone begins to be produced to a lesser extent and an increased secretion of sebum can be observed.
  2. Fungi. Malassezia yeast can cause dandruff to break down sebum into oleic acid, which can irritate the sensitive scalp and cause itching and flaking.This sensitivity is observed in 50% of the world’s population.
  3. Individual features. Genetic predisposition to the disease, the structure of the skin and its secretion. People with comorbid skin conditions such as psoriasis and eczema are more likely to suffer from dandruff than others. Mental stress, malnutrition, concomitant diseases that affect immunity.

How is it treated?

Antifungal agents are used to treat dandruff – special shampoos, lotions.

It is also recommended to consult a trichologist. Based on the results of the examination and the collection of anamnesis, additional consultations of related specialists can be assigned. Since the appearance of dandruff is often associated with a weakened immune system and pathologies of the gastrointestinal tract, it is also necessary to consult an immunologist, gastrointerologist, infectious disease specialist.

When treating seborrhea, you must first find out and eliminate the causes of the disease. It is better to consult a trichologist to find out the severity and the selection of drugs for the treatment of your particular case.Since with seborrhea there is a violation of the activity of the sebaceous gland, which is located in the lower layers of the epidermis, the treatment should be aimed at reducing sebum production, that is, to be “intradermal”.

Shampoo is necessary in order to wash off the sebaceous secretion from the surface of the scalp, therefore, in combination with it, it is necessary to use sebum-regulating masks or lotions that are kept on the head for 20-30 minutes. The diet should be balanced: limit the consumption of sweet, fatty foods.Food should be rich in fiber to improve digestion, vitamins, fermented milk products.

Arpimed

Shampoo is applied to the affected areas, do not rinse for 3-5 minutes, then rinse with water.

When treating dandruff and seborrheic dermatitis, shampoo is applied to the scalp 2 times a week for 3-4 weeks; with pityriasis versicolor – daily for 5 days.

For the prevention of dandruff and seborrheic dermatitis, use once a week or once every 2 weeks; with pityriasis versicolor, 1 time / day for three days before the onset of summer.

Side effects

As with other shampoos, local irritation, itching or contact dermatitis (due to irritation or allergic reaction) may occur. Hair can become oily or dry. However, when using ketoconazole 2% shampoo, such phenomena are rare.

In some cases, mainly in patients with chemically damaged or gray hair, there was a change in hair color.

Adverse reactions identified during clinical trials: Adverse reactions observed in ≥ 1% of patients after applying ketoconazole shampoo 2% to the scalp or skin were not identified.Adverse reactions observed in ≤ 1% of patients applying ketoconazole shampoo to the scalp or skin are listed below:

From the side of the organs of vision: eye irritation, increased lacrimation.

Systemic disorders and complications at the injection site: erythema at the site of application, irritation at the site of application, hypersensitivity, pruritus, pustules, skin reactions.

Immune system disorders: hypersensitivity.

Infections and invasions : folliculitis.

From the nervous system: violation of taste sensitivity.

Skin and subcutaneous tissue disorders: acne, alopecia, contact dermatitis, dry skin, disturbed hair texture, burning sensation, skin rash, skin peeling.

Adverse effects identified during post-marketing studies are listed below according to the following classification:

Very often ≥ 1/10

Often ≥ 1/100 and ≤ 1/10

Uncommon ≥ 1/1000 and ≤ 1/100

Rare ≥ 1/10000 and ≤ 1/1000

Very rare <1/10000, including single messages

Skin and subcutaneous tissue disorders:

Very rare: edema, urticaria, hair color change.

90,000 Analyzes at KDL. Allergic complex for eczema-2

Eczema is an inflammatory reaction of the skin, which develops as a response of the immune system to the effects of various external and internal factors. There is an acute and chronic form of eczema. Typical symptoms include a rash that is itchy and burning and tends to recur (reappear). Eczema often occurs with atopic dermatitis, a common allergic disease.Often, eczema occurs in early childhood and can become chronic, which persists in adults (sometimes throughout life).

Symptoms of eczema and atopic dermatitis are similar to manifestations of other skin diseases (caused by infections or parasites), as well as diseases of internal organs (liver, kidneys, gastrointestinal tract, nervous system, hormonal disorders). All this complicates the diagnosis, therefore, to find out the causes of skin lesions, various tests for sensitivity to allergens are used, among other things.One of these tests is the allergic complex for eczema-2 developed by KDL, which reveals the sensitivity of the patient’s body to a wide range of skin allergens. Among them are dandruff and epithelium of cats and dogs, house dust mites, egg yolk and white, milk, wheat, soybeans, cod and cocoa. According to the recommendations of the EAACI (European Academy of Allergology and Clinical Immunology), tests for the above allergens are recommended for children and adults when symptoms of eczema and other skin rashes appear.

In what cases is the study usually prescribed?

The analysis is prescribed in the presence of skin rashes in adults and children with burning, itching, redness, dryness and flaking, with symptoms of food allergies, as well as in the differential diagnosis of the causes of eczema.

What exactly is determined in the analysis process?

This study determines the presence of specific immunoglobulins – IgE to the main household, skin, pollen and food allergens using the ImmunoCAP method.

  • cat, epithelium and dandruff,
  • dog, dandruff,
  • house dust mite D1,
  • egg yolk,
  • egg white,
  • milk,
  • wheat,
  • soy,
  • cod,
  • cocoa

ImmunoCAP technology is highly accurate and specific /

What do the test results mean?

A positive result indicates that the patient has become sensitized to one or more of the tested allergens, and his immune system perceives this substance as an antigen and produces immunoglobulins E in response to contact with the allergen, which leads to symptoms of eczema.A negative result indicates a lack of sensitization (sensitivity) to the allergen

Timing of the test.

Typically, the test result can be obtained within 7-8 days.

How do I prepare for the analysis?

The general rules of preparation for taking blood from a vein should be adhered to. Detailed information can be found in the corresponding section of the article.

Treatment of seborrheic dermatitis, pityriasis versicolor, etc.

Pityriasis versicolor

Pityriasis versicolor or Colorado verse is a fungal skin disease that affects the stratum corneum of the epidermis.Sweating, hot climate, seborrheic skin conditions are predisposing factors for the onset of pityriasis versicolor. The incidence of pityriasis versicolor is higher in women and young people. Outbreaks of infection and relapses of pityriasis versicolor are recorded in the hot season. Infection occurs in a contact-household way through the use of common combs, household items, as well as through direct contact between a sick person and a healthy person.

Pityriasis versicolor begins with the appearance of a single rounded pink spot, then the same spots, but of a smaller diameter, appear on the smooth skin and scalp.With pityriasis versicolor, skin changes are non-inflammatory in nature, the spots are usually yellowish-brown in color, and when they are scraped, slight pityriasis peeling is noted. Pityriasis lichen spots are prone to peripheral growth and fusion, itching and other subjective sensations are absent.

Compliance with the rules of personal hygiene is the only prevention of pityriasis versicolor. It is impossible to completely get rid of mycotic cells, and therefore in the spring time you should use cosmetics with an antifungal effect and avoid sun exposure to prevent relapse.

Seborrheic eczema

Seborrheic eczema – chronic dermatosis, manifested by rashes of small nodules, gradually forming plaques, covered with dense fatty scales and crusts, when removed, a moist surface opens. Rashes of seborrheic eczema are localized on the head, behind the ears, on the face, in the natural folds of the skin, in the umbilical region, on the skin of the trunk and flexor surfaces of the arms and legs. It is one of the clinical forms of eczema.The disease can occur equally in persons of both sexes and any age. Often seborrheic eczema develops against the background of seborrhea or as a complication of seborrheic dermatitis. In HIV-infected people, it can be one of the first manifestations of AIDS. A feature of seborrheic eczema in such patients is its spread throughout the skin.

Causes of seborrheic eczema

Factors predisposing to the development of seborrheic eczema are increased production of secretion by the sebaceous glands, gastrointestinal diseases (gastritis, peptic ulcer), abnormalities in the liver (hepatitis, cirrhosis), hormonal abnormalities (diabetes mellitus, imbalance of estrogens and androgens, obesity), vegetative-vascular dystonia.It is noted that seborrheic eczema often occurs against a background of reduced immunity, which in turn may be due to frequent acute respiratory viral infections, a severe illness, a chronic infectious focus (sinusitis, sinusitis, otitis media, tonsillitis, etc.).

Symptoms of seborrheic eczema

Seborrheic eczema begins with small, pink-yellow nodules on the skin. The nodules increase and merge with each other, which leads to the formation of infiltrated disc-shaped plaques.The plaques are 1–2 cm in diameter and are covered with numerous dense fatty scales. When removing the scales, a slightly damp surface opens under them, pronounced weeping is not typical.

The lesions of seborrheic eczema have clear boundaries and uneven edges. At the onset of the disease, they may be dry, but then take on a typical “greasy” appearance. Itching, as a rule, is mild and does not bother patients much.

Usually rashes of seborrheic eczema are located on the head: in the hair growth zone, on the forehead, in the eyebrows, in the nasolabial folds, around the mouth and behind the ears.With the localization of foci of seborrheic eczema on the scalp, they, growing along the periphery, eventually move to the edge of hair growth and to the forehead.

With seborrheic eczema, the skin of the eyelids is often affected with the development of blepharitis

Diagnosis of seborrheic eczema

The diagnosis of seborrheic eczema is established by a dermatologist. Often, a visual examination of skin lesions is sufficient for this. They also carry out dermatoscopy, fluorescent diagnostics, examination of skin and hair scrapings for pathogenic fungi

To identify underlying diseases and foci of chronic infection, patients with seborrheic eczema may be assigned consultations of other specialists: gastroenterologist, endocrinologist, gynecologist, otolaryngologist, neurologist.For the same purpose, additional examinations are carried out: gastroscopy, ultrasound of the abdominal organs, hormonal and immunological blood tests, ultrasound of the small pelvis, rhinoscopy, pharyngoscopy, etc. Patients with lesions of the eyelids need an ophthalmologist’s consultation.

Recommendations

Patients with increased sebum secretion are advised to limit the use of fatty, fried, sweet and spicy foods, avoid going to the bathhouse and staying in a humid and hot climate.